Wild blueberry (Vaccinium angustifolium) is a perennial plant native to North America. This berry is rich in polyphenols, particularly flavonoids, which offer significant health benefits. A recent study published in Critical Reviews in Food Science and Nutrition provides a comprehensive review of the evidence and insights shared at an expert symposium regarding wild blueberries and their link to cardiometabolic health.
Vaccinium angustifolium. Image credit: Σ64 / CC BY 3.0.
Known for their high nutrient content, wild blueberries, or lowbush blueberries, are celebrated for their abundance of anthocyanins and other beneficial compounds.
These polyphenols, contributing to the berries’ vibrant blue hue, have been thoroughly researched for their powerful antioxidant properties.
“Wild blueberries have been valued for centuries,” noted University of Maine professor Dorothy Krimis Zakas, co-lead author of the recent review.
“Traditional wisdom recognizes their significance, and modern research continues to investigate how the unique constituents of wild blueberries contribute to health when part of a balanced diet.”
This review analyzed 12 human clinical trials conducted across four countries and numerous additional studies on the health effects of compounds found in wild blueberries.
The most consistent result from these studies was an improvement in vascular function, indicating better blood vessel responsiveness.
Some trials noted enhanced endothelial function just hours after consuming wild blueberries, while others observed benefits from regular intake over longer periods.
Recent studies have also highlighted the impact of wild blueberries on the gut microbiome.
Thanks to their high fiber and polyphenol content, these berries resist early digestion and are processed by gut bacteria into metabolites that enter the bloodstream.
These metabolites can constitute a significant proportion of bioactive compounds in circulation post-consumption; one study demonstrated that daily intake of freeze-dried wild blueberry powder boosted levels of beneficial bioactive compounds such as Bifidobacterium.
Emerging evidence suggests that consistent blueberry consumption may enhance cognitive abilities, especially thinking speed and memory in older adults, possibly linked to improved circulation and other systemic effects.
For adults at higher cardiometabolic risk, several studies referenced in the review identified meaningful improvements in blood pressure, glycemic control, and lipid profiles, including reductions in total cholesterol, LDL (bad) cholesterol, and triglycerides, following weeks of regular blueberry intake.
“What’s remarkable about wild blueberries is their wealth of polyphenols and nutrients. Their health benefits appear to stem from multiple mechanisms,” explained Sarah A. Johnson, Ph.D., from Florida State University, co-lead author of the review.
“Evidence indicates that these berries may influence various biological pathways related to cardiometabolic health, including vascular function and inflammation, but individual responses may vary.”
“The recent focus on the gut microbiome’s role in health benefits is intriguing and might help researchers understand how to optimize gut health for enhanced wellness.”
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Sarah A. Johnson et al. Wild blueberries and cardiometabolic health: A current review of the evidence. Critical Reviews in Food Science and Nutrition, published online January 24, 2026. doi: 10.1080/10408398.2025.2610406
Researchers exploring solutions for Inflammatory Bowel Disease (IBD) have drawn surprising inspiration from barnacles.
Inflammatory Bowel Diseases, including Crohn’s disease and ulcerative colitis, typically arise when the immune system mistakenly attacks the intestines, leading to inflammation. Common symptoms encompass diarrhea, significant abdominal pain, weight loss, and gastrointestinal bleeding.
While anti-inflammatory medications like steroids can alleviate symptoms, persistent bleeding may necessitate the use of small metallic clips inserted into the intestine to address the inflammation-induced wounds. However, this procedure carries potential infection risks and may exacerbate the injury.
In pursuit of gentler alternatives, researchers have previously engineered bacteria to generate proteins beneficial for wound healing. Unfortunately, these microorganisms are generally eliminated from the intestines within days and require manual activation with pharmaceuticals, according to Bolin Anne from the Shenzhen Institute of Synthetic Biology in China.
Recently, Ahn and colleagues have genetically modified a benign strain of Escherichia coli that produces protein fragments promoting wound healing upon detecting blood. They also engineered these bacteria to create a type of “cement protein” used by barnacles to adhere to submerged surfaces, envisioned as a “living glue” to fabricate an anti-inflammatory seal over open wounds.
To validate this novel approach, researchers induced intestinal inflammation and scarring in mice. Each subject received either a non-genetically engineered strain, the engineered Escherichia coli, or saline via an anal tube.
After ten days, mice treated with the engineered bacteria exhibited significant weight restoration, and their intestines mirrored the health of uninjured mice. No adverse side effects were recorded in any group.
Similar outcomes were noted when bacteria were administered in tablet form, suggesting potential for oral delivery in human treatment. “This presents a promising, innovative strategy,” states Shaji Sebastian at Hull University in the UK. He indicates that wound healing and inflammation in the mouse intestine is analogous to processes in humans, underscoring the necessity for human trials.
Plans are underway to test this approach in larger animals, including pigs, to assess how long the genetically modified bacteria remain viable in the gut, Ang mentioned. However, due to the necessity for extensive testing to confirm efficacy and safety compared to existing treatments, it may take up to ten years before these solutions could become available in clinics, according to Sebastian.
Greenland Sharks’ Longevity: A Closer Look at Their Heart Health
Credit: Doug Perrine/naturepl.com
Greenland sharks are believed to live between 250 to 500 years. Remarkably, even at 150 years old, they show signs of severe age-related heart disease.
Interestingly, some body parts like their eyes seem resilient to aging and cancer, suggesting that not all organs in this ocean predator are equally affected by age. Despite this resilience, research has shown that Greenland sharks (Somniosus microcephalus) do have significant heart health issues, yet they show no obvious functional decline or reduced lifespan.
Alessandro Cellerino and his team at the École Normale Supérieure in Pisa, Italy, conducted a study on six Greenland sharks (four females and two males), each exceeding 3 meters in length, and found their results to be “truly surprising.”
The researchers estimate that all six specimens were between 100 and 150 years old. They employed various advanced microscopic techniques, including high-resolution fluorescence and electron microscopy, to investigate the animals’ heart tissues.
“The hearts of Greenland sharks exhibited significant fibrotic changes and an abundance of aging markers such as lipofuscin and nitrotyrosine,” stated Cellerino.
In humans, elevated fibrosis levels in heart tissues typically signal age-related heart problems and potential heart failure.
Nevertheless, Cellerino noted that the substantial accumulation of lipofuscin, associated with mitochondrial impairment, does not appear detrimental and “does not adversely affect the lifespan of Greenland sharks.”
The high levels of nitrotyrosine, another marker associated with heart inflammation and oxidative stress, suggest that Greenland sharks may have developed a unique evolutionary strategy for enduring chronic oxidative damage, as opposed to merely attempting to avoid it.
“Initially, I thought what I observed under the microscope was a technical artifact or an error in the experiment,” he remarked.
To compare, the researchers also examined another deep-sea fish, the velvet-bellied lantern shark (Etmopterus spinax), along with the turquoise killifish (Nosobranchius furzeri), a species noted for its fleeting lifespan of mere months, residing in seasonal pools across the African savannah.
Elena Chiavatti mentioned that while the Greenland shark’s heart is highly fibrotic, the other species showed no signs of such conditions, as indicated in the Scuola Normale Superiore paper.
“The accumulation of nitrotyrosine is significant in Greenland sharks, whereas lantern sharks show no accumulation,” Chiavatti commented.
Despite their brief lifespans, killifish share similar nitrotyrosine aging markers with Greenland sharks, she added.
Cellerino emphasized that Greenland sharks exhibit extraordinary resilience to aging, particularly in their hearts. “The existence of organisms like Greenland sharks that endure aging without any noticeable heart decline is remarkable,” he noted. “These findings underscore the exceptional heart resilience of Greenland sharks and suggest potential insights into healthy aging.”
João Pedro Magalhães from the University of Birmingham highlighted that the study underscores our limited understanding of the molecular and cellular aging mechanisms, including which changes are detrimental and which are advantageous.
Furthermore, Magalhães urged for a broader variety of animals in aging and lifespan research. “Most scientists, including myself, primarily use short-lived species like earthworms, mice, and rats, but remarkable long-lived species such as Greenland sharks and bowhead whales could hold the keys to longevity,” he urged.
Alzheimer’s disease presents significant challenges, transforming a cherished family member into someone who often fails to recognize their true self. Many individuals ponder the reasons behind the erosion of memories and personalities. Researchers have identified the primary driver of Alzheimer’s as the accumulation of a brain protein known as Tau.
Under normal circumstances, tau protein plays a crucial role in preserving the health of nerve cells by stabilizing the microtubules, which function as pathways for nutrient transport. However, in Alzheimer’s patients, tau protein becomes twisted and tangled, obstructing communication between cells. These tau tangles are now recognized by medical professionals as a defining characteristic of Alzheimer’s disease, serving as indicators of cognitive decline.
Recent studies have shown that tau tangles correlate with diminished brain function in individuals affected by Alzheimer’s disease. Additionally, the apolipoprotein E4 (APOE4) gene is closely linked to late-onset Alzheimer’s and may exacerbate tau tangling. This gene encodes a protein involved in transporting fats and cholesterol to nerve cells throughout the brain.
A team from the University of California, San Francisco, and the Gladstone Institute has discovered that eliminating APOE4 from nerve cells can mitigate cognitive issues associated with Alzheimer’s. Their research involved specially bred mice exhibiting tau tangles and various forms of the human APOE gene, specifically APOE4 and APOE3. The aim was to determine if APOE4 directly contributes to Alzheimer’s-related brain damage and if its removal could halt cognitive decline.
To investigate the impact of the APOE4 gene, the researchers introduced a virus containing abnormal tau protein into one side of each mouse’s hippocampus. When the mice reached 10 months of age, the team conducted various tests—including MRI scans, staining of brain regions, microscopy, brain activity assessments, and RNA sequencing—to analyze the accumulation of tau protein in the brains of those with and without the APOE4 gene.
The findings revealed significant discrepancies between the two groups. Mice with the APOE4 gene displayed a higher prevalence of tau tangles, a marked decline in brain function, and increased neuronal death, while those with the APOE3 gene exhibited minimal tau deposits and no cognitive decline.
Next, the researchers employed a protein linked to an enzyme called CRE to excise the APOE4 gene from mouse nerve cells, subsequently measuring tau levels with a specialized dye. The results indicated a significant reduction in tau tangles, dropping from nearly 50% to around 10%. In contrast, mice carrying the APOE3 gene saw an even smaller reduction from just under 10% to approximately 3%.
Additionally, a different dye was utilized to quantify amyloid plaques—another protein cluster frequently found in Alzheimer’s cases. The outcomes showed that, following removal of the APOE4 gene, amyloid plaque levels decreased from roughly 20% to less than 10%. Mice with the APOE3 gene, however, displayed no notable change, consistently maintaining around 10% amyloid plaques.
The researchers further analyzed the RNA of the mice to understand how APOE4 affects neurons and other brain cells. Their observations confirmed that the presence of APOE4 correlated with an uptick in Alzheimer’s-related brain cells. This finding helped illustrate that eliminating APOE4 from nerve cells resulted in diminished responses associated with Alzheimer’s disease.
In conclusion, the researchers determined that APOE4 is detrimental and may actively induce Alzheimer’s-like damage in the brains of mice. While further validation in human subjects is needed, the implications of this gene may pave the way for developing targeted therapies for Alzheimer’s disease.
Alzheimer’s Disease (AD) has long been deemed irreversible. However, a groundbreaking study by scientists from Case Western Reserve University, University Hospitals, and the Louis Stokes Cleveland VA Medical Center reveals that treatment for advanced Alzheimer’s disease can be reversed. Through extensive research on both preclinical mouse models and human brain samples, the team discovered that the brain’s failure to maintain normal levels of nicotinamide adenine dinucleotide (NAD+), the crucial energy molecule of cells, significantly contributes to the onset of Alzheimer’s. Furthermore, sustaining an appropriate NAD+ balance may not only prevent but also reverse the progression of Alzheimer’s disease.
Alzheimer’s disease severity correlates with NAD+ homeostatic dysregulation. Image credit: Chaubey et al., doi: 10.1016/j.xcrm.2025.102535.
Historically, Alzheimer’s disease, the primary cause of dementia, has been regarded as irreversible since its identification over a century ago, and it is expected to impact more than 150 million individuals globally by 2050.
Current therapies focused on amyloid beta (Aβ) and clinical symptoms offer limited benefits, underscoring the urgent need for complimentary and alternative treatment options.
Intriguingly, individuals with autosomal dominant AD mutations can remain symptom-free for decades, while others without Alzheimer’s neuropathology maintain cognitive function despite having numerous amyloid plaques.
These insights indicate potential intrinsic brain resilience mechanisms that may slow or halt disease progression, suggesting that enhancing these processes could enhance recovery from Alzheimer’s disease.
NAD+ homeostasis plays a pivotal role in cellular resilience against oxidative stress, DNA damage, neuroinflammation, blood-brain barrier degradation, impaired hippocampal neurogenesis, deficits in synaptic plasticity, and overall neurodegeneration.
In a recent study, Professor Andrew Pieper and his team from Case Western Reserve University discovered that NAD+ levels decrease significantly in the brains of Alzheimer’s patients, a trend also observed in mouse models.
While Alzheimer’s disease is unique to humans, it can be effectively modeled using genetically engineered mice that carry mutations linked to human Alzheimer’s disease.
The researchers utilized two distinct mouse models: one with multiple human mutations affecting amyloid processing and another with a human mutation in the tau protein.
Both models exhibited Alzheimer’s-like brain pathology, including blood-brain barrier degradation, axonal degeneration, neuroinflammation, impaired hippocampal neurogenesis, diminished synaptic transmission, and excessive oxidative damage.
They also developed cognitive impairments typical of Alzheimer’s patients.
Upon discovering the sharp decline in NAD+ levels in both humans and mice with Alzheimer’s, the scientists investigated whether preserving NAD+ levels before disease onset and restoring them after significant disease progression could prevent or reverse Alzheimer’s.
This research builds upon prior work showing potential recovery by restoring NAD+ balance following severe brain injuries.
The team achieved NAD+ balance restoration using a well-known pharmacological agent, P7C3-A20.
Remarkably, maintaining NAD+ balance not only shielded mice from developing Alzheimer’s but also enabled brain recovery from key pathological changes even when treatment was delayed in advanced disease stages.
Subsequently, both mouse strains fully regained cognitive function, accompanied by normalized levels of phosphorylated tau-217—a recently recognized clinical biomarker for Alzheimer’s disease in humans—confirming the restoration of cognitive function and highlighting a potential biomarker for future Alzheimer’s disease reversal trials.
“We are excited and hopeful about these results,” said Professor Pieper.
“Restoring brain energy balance led to both pathological and functional recovery in mice with advanced Alzheimer’s disease.”
“Observing this effect across two different animal models, driven by distinct genetic causes, reinforces the notion that recovery from progressive Alzheimer’s disease may be achievable through the restoration of brain NAD+ balance.”
These findings encourage a shift in how researchers, clinicians, and patients perceive treatment options for Alzheimer’s disease moving forward.
“The key takeaway is one of hope. Alzheimer’s disease effects may not necessarily be permanent,” noted Professor Pieper.
“Under certain conditions, the damaged brain can self-repair and regain functionality.”
“Through our research, we not only demonstrated a drug-based method for promoting recovery in animal models but also identified candidate proteins in human AD brains that may aid in reversing the disease,” remarked Dr. Kalyani Chaubey, a researcher at Case Western Reserve University and University Hospitals.
While current commercially available NAD+ precursors have been shown to elevate cellular NAD+ to unsafe levels—potentially promoting cancer—the pharmacological approach of this study employs P7C3-A20, which allows cells to maintain optimal NAD+ levels under stress without elevating them excessively.
“This is a crucial consideration for patient care, and clinicians should explore therapeutic strategies aimed at restoring the brain’s energy balance as a viable path toward disease recovery,” Professor Pieper concluded.
For more detailed information, see the study findings published in Cell Reports Medicine.
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Kalyani Chaubey et al. Pharmacological reversal of advanced Alzheimer’s disease in mice and identification of potential therapeutic nodes in the human brain. Cell Reports Medicine, published online on December 22, 2025. doi: 10.1016/j.xcrm.2025.102535
Huntington’s Disease: A Gradual Destruction of Brain Cells.
Science Photo Library/Alamy
This year marks a watershed moment in addressing Huntington’s disease, a rare yet impactful form of dementia. Researchers have achieved a groundbreaking milestone with an experimental gene therapy that effectively slows the advancement of this debilitating condition for the first time ever. This represents a significant breakthrough in the search for viable treatments.
According to Sarah Tabrizi from University College London, “This is a monumental step forward,” referencing the successes observed in late-stage trials earlier this year. “We now understand that Huntington’s disease is potentially treatable, presenting us with a tremendous opportunity.”
Huntington’s disease stems from a genetic mutation that causes the normally benign huntingtin protein to cluster into harmful aggregates within the brain. This accumulation leads to gradual deterioration of brain cells, hindering movement, cognitive function, and emotional well-being. Currently, no approved treatments halt the progression of symptoms, and care primarily focuses on supporting affected individuals.
The novel treatment, dubbed AMT-130, directly targets these abnormal proteins by delivering genetic instructions to brain cells, instructing them to produce molecules that inhibit protein formation.
In a recent investigation, Tabrizi and her team administered high doses of AMT-130 to 17 patients with Huntington’s disease. They evaluated changes in cognitive, motor, and daily functioning over a three-year period compared to a control group. Preliminary results released by the drug’s manufacturer, biotechnology firm uniQure, indicate a remarkable 75% average slowdown in symptom progression.
“Huntington’s disease treatment has faced numerous challenges in recent years,” stated Sarah O’Shea at Mount Sinai in New York, who was not involved in the study. “This accomplishment is significant, not just in delaying the disease’s progression but also because it arrives at a crucial time when hope is desperately needed.”
Nevertheless, this innovative treatment does come with its own set of challenges. Tabrizi explained that the 12- to 18-hour surgical procedure required to deliver the treatment deep within the brain is only accessible in a limited number of facilities in select countries, including the U.S. and U.K. Additionally, if approved, the treatment is likely to be prohibitively expensive. “Will it be accessible to all? Achieving that will be a challenge,” she remarked.
To navigate these hurdles, Tabrizi and her team are developing an alternative therapy that involves injecting the fluid around the spinal cord. “We’re currently conducting a Phase I study, and the first patient was treated in November 2024,” Tabrizi noted, with safety results expected by July 2026.
Meanwhile, uniQure’s executives revealed in September plans to submit AMT-130 for FDA approval in early 2026. However, the submission timeline is now uncertain, as the FDA has expressed concerns regarding the study plan and the control group, which consists of *non-treatment* patients drawn from a database.
The absence of a proper control group complicates the ability to discern the placebo effect on results. Still, given the surgical nature of the treatment, establishing such a group poses significant challenges.
“We firmly believe that AMT-130 holds substantial potential to benefit patients and are dedicated to collaborating with the FDA to expedite access to this treatment for families in need across the U.S.,” stated Matt Kapusta, CEO of uniQure.
Life encompasses more than mere figures, yet it often seems otherwise in today’s world. We exist in a time dominated by wearable tech, health tracking, and extreme optimization.
With just a few unobtrusive devices, driven individuals can transform themselves into intelligent data compilers.
We can keep an eye on blood oxygen levels, breathing rates, blood sugar, REM sleep, skin temperature, heart rate variability, body composition, and an array of other biomarkers regularly.
If desired, you can document your meals, mood, menstrual cycles, and even bowel habits.
The goal is to have access to all this information so we can enhance and extend our lives. But how do we extract significance from it?
How can we gain genuine health insights without dedicating hours to computations and organization? Because aside from a few bored billionaires, most of us don’t view our living spreadsheets as truly valuable.
Fortunately, researchers at Northwestern University in the US have some exciting news. In 2025, they discovered a method to: Combine two commonly measured health indicators to provide us with deeper insights into daily fitness and long-term health risks.
The daily heart rate per step (DHRPS) is a straightforward measure. Simply divide your average daily heart rate by your average step count.
Yes, you’ll need to constantly track both metrics using a health monitor, such as an Apple Watch or Fitbit (the latter being utilized in the research), but the calculations are done automatically.
In just 2 seconds, you can uncover critical information about your cardiovascular health.
“We discovered that [DHRPS measurement] has a stronger correlation with type 2 diabetes, heart failure, myocardial infarction, and heart attacks,” said Flynn Chen, the lead author of the paper. “It’s significantly more informative than merely tracking heart rate or steps.”
Improving Your Score
Here’s the breakdown: Suppose your average heart rate for the month is 80 beats per minute, and you walk an average of 6,000 steps daily. Your DHRPS score would then be 0.01333.
Now, if you boost your step count to an average of 10,000 steps per day over the following month, your DHRPS should drop to 0.008. In this case, a lower score is preferable.
In their study, Chen and colleagues monitored over 7,000 Fitbit users across five years, during which they recorded more than 50 billion steps.
Taking more steps can effectively benefit your overall health – Photo credit: Getty
The researchers categorized participants into three groups based on their DHRPS scores: low (below 0.0081), moderate (above 0.0081 and below 0.0147), and high (above 0.0147).
The simplest way to alter your score is by increasing your step count, Chen suggests.
“Numerous established studies indicate that daily step count is an independent risk factor for cardiovascular disease and overall mortality,” he adds.
“Our ongoing research reveals that heart rate in relation to step count may be an even stronger independent risk factor for cardiovascular disease than step count alone.
“By increasing your step count, you not only pursue the 10,000 steps daily goal, but also improve both metrics simultaneously.”
Chen advises that you need at least a week’s worth of consistent data from your smartwatch or tracker for a meaningful DHRPS score.
The Future of Heart Rate per Step
Since the release of this study, the health tracking community has started utilizing these insights, potentially leading to further advancements as more data becomes available.
“A crucial aspect is that our metrics correlate with VO.2 max scores,” Chen mentions.
This is significant because V.O.2 maximum measures the highest rate of oxygen consumption during exercise, providing valuable insights regarding your aerobic capacity and metabolic health.
The challenge lies in accurately measuring VO.2 max, as it typically requires a treadmill stress test, with limited availability of such tests.
If DHRPS proves to be a reliable indicator of VO.2 max, it could serve as another method to simplify health data access for everyone—no spreadsheets needed.
Ulcerative colitis is characterized by inflammation of the colon and rectum lining.
BSIP SA/Alamy
Toxins from bacteria in contaminated water can destroy immune cells in the colon’s lining. This implies that individuals whose intestines host these bacteria are significantly more likely to develop ulcerative colitis.
This conclusion is derived from a series of studies undertaken with both humans and animals by Shwena Chan and colleagues at Nanjing University, China. If validated, these findings could pave the way for new treatment options.
Ulcerative colitis is one of the primary types of inflammatory bowel disease (IBD), marked by inflammation of the colon and rectum lining. Symptoms typically fluctuate between periods of remission and flare-ups, sometimes necessitating the removal of the colon in severe cases.
The exact cause of ulcerative colitis remains unclear, although it is often regarded as an autoimmune disorder influenced by both genetic and environmental factors. Chan’s team theorized that immune cells called macrophages might be integral to the condition.
Macrophages are found throughout various body tissues, performing the dual roles of clearing debris and bacteria while regulating local immune responses. They can signal additional immune cell recruitment and initiate inflammation but are equally important in mitigating it.
Researchers discovered that the density of resident macrophage cells was notably reduced in colon tissue from patients with ulcerative colitis compared to those without the condition. Further experimentation demonstrated that depleting macrophages in mice increased their susceptibility to colitis, suggesting that losing macrophage protection leads to colon damage and inflammation.
But what accounts for the lower macrophage levels in ulcerative colitis patients? By analyzing fecal samples, the research team identified a toxin named aerolysin, which significantly harms macrophages while sparing other intestinal cells.
Aerolysin is secreted by several strains of bacteria belonging to the genus Aeromonas, frequently found in freshwater and brackish environments. The strains responsible for producing aerolysin are referred to as MTB (macrophage-toxic bacteria).
In experiments where mice were deliberately infected with MTB, they exhibited greater vulnerability to colitis. Conversely, even after removing the aerolysin gene from the bacteria or neutralizing the toxin with antibodies, the mice did not show increased susceptibilities to the condition.
Ultimately, the research team tested for Aeromonas in stool samples, discovering its presence in 72% of the 79 patients with ulcerative colitis, versus only 12% among 480 individuals without the condition. This test, however, could not confirm if these bacteria were indeed MTB or if they produced aerolysin.
The findings offer a nuanced perspective. Not every case of ulcerative colitis is linked to MTB, and some individuals can carry MTB without developing the disease.
“We cannot assert that MTB is the exclusive cause of ulcerative colitis,” Zhang states. “Ongoing MTB infection can create a hypersensitive environment in the colon, yet not everyone infected will develop colitis.”
“Environmental and genetic factors certainly influence the emergence of colitis,” she adds.
According to Zhang, there are at least three potential approaches for new treatment development. One involves creating drugs to neutralize the toxin; another would focus on vaccines targeting the toxin or the bacteria producing it; while a third approach seeks to eradicate toxin-producing bacteria via phage therapy, which utilizes viruses that selectively kill specific bacteria.
“The leading theory posits that MTB toxin depletes specialized macrophages in the intestinal lining, undermining intestinal immunity,” explains Dr. Martin Kriegel from the University Hospital of Münster, Germany.
He has observed that when the team eradicated all intestinal bacteria in mice and subsequently infected them with MTB, their susceptibility to colitis diminished. This observation indicates that other yet-to-be-identified bacterial species could also play a role.
“Nonetheless, this may represent a crucial, overlooked factor in the multi-step development of ulcerative colitis, especially in China,” Kriegel suggests.
Zhang and her research group intend to conduct more extensive epidemiological studies to substantiate the association between MTB and ulcerative colitis. If MTB infection is confirmed and becomes increasingly prevalent, it may elucidate the rising incidence of IBD.
A hibernating species of North American squirrel might provide vital insights for tackling one of the most persistent and lethal heart diseases globally.
California’s biotechnology firm fauna ecology has created a novel drug based on the genetic insights of hibernating mammals.
The small molecule drug, referred to as Faun 1083, targets heart failure with preserved ejection fraction (HFpEF)—a form of heart failure impacting millions and lacking effective treatments.
Fauna’s strategy draws inspiration from the natural world, as noted by CEO Dr. Ashley Zehnder: “We’re investigating where biological evidence exists for disease resistance or recovery,” as mentioned in BBC Science Focus.
“Years of physiological research indicate that ground squirrels can safeguard their hearts from harm during hibernation. Additionally, heart failure ranks as one of the top causes of death worldwide.”
By examining how the adorable American line squirrel protects its organs while hibernating, Dr. Fauna discovered a gene that aids the animal in averting tissue damage and scarring—critical factors in heart failure among humans.
“What is elevated in the ground squirrel’s system, which shields the heart from harm, may be diminished in humans suffering from heart failure,” Zehnder explains. “This informs our focus on the pathways that are crucial for human health issues.”
Currently, there are limited effective treatments for heart failure with preserved ejection fraction (HFpEF) beyond merely alleviating symptoms – Photo credit: Getty
Fauna’s AI-enhanced discovery platform analyzes these protective traits across animal genomes and human genetic data to identify potential drug targets.
According to Zehnder, the resultant compound Faun 1083 stems directly from research into the cardiac biology of ground squirrels. The new treatment has already shown potential during preclinical trials and is set to undergo animal safety assessments prior to commencing human trials next year.
Fauna Bio’s research is part of a burgeoning field known as ‘comparative genomics,’ which seeks evolutionary insights to enhance human health.
The company is part of the Zoonomia Consortium, which unveils adaptations that enable animals to resist disease and recover from tissue damage.
“Our goal is to leverage evolutionary adaptations,” Zehnder asserts. “Humans rarely cure diseases naturally, but many mammals worldwide do so regularly… Why not utilize the full spectrum of nature’s experiments?”
Vaccination against covid-19 is safer than infection
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Recent findings highlight that vaccinating children is more beneficial than exposing them to the coronavirus. A comprehensive study involving nearly 14 million children revealed that the likelihood of experiencing serious, albeit uncommon, side effects related to the heart and blood vessels was considerably greater following an infection compared to a vaccination.
Specifically, children aged 5 to 18 experienced 17 additional infections per 100,000 with inflammatory conditions such as Kawasaki disease in the six months after contracting SARS-CoV-2, as opposed to other periods. Conversely, among children first vaccinated with the Pfizer/BioNTech mRNA vaccine, infections per 100,000 dropped by almost two.
Myocarditis, which is inflammation of the heart muscle, resulted in over two extra cases per 100,000 individuals in the six months post-infection. In comparison, there was less than one additional case among vaccinated individuals, indicating that the risk of myocarditis is more than double following infection relative to vaccination.
A report highlighting a new coronavirus infection causing myocarditis has been made known. As early as April 2020, reports began surfacing even after vaccinations commenced in December. Vaccines associated with myocarditis tend to present milder symptoms, particularly in young men, and most individuals recover swiftly.
The uncommon side effects of this vaccine have garnered substantial media focus and stirred significant concern, contributing to delays in introducing routine childhood vaccinations in the UK until April 2022.
The latest findings reinforce earlier research indicating that vaccinated children face a lower risk of myocarditis compared to their unvaccinated peers, despite the rarity of this side effect. A majority of children contracted the virus, placing them at an elevated risk of adverse effects.
“It’s important to note that severe complications are highly uncommon among children and adolescents in general,” states Angela Wood from Cambridge, UK, a part of the HDR UK regional network. “Nevertheless, evidence suggests that the risk is generally higher following COVID-19 compared to vaccination.”
Wood’s team evaluated data from the UK’s National Health Service (NHS) encompassing approximately 14 million children under 18 from January 2020 to December 2021. During the latter half of this timeframe, 3.9 million children received the Pfizer/BioNTech vaccine, while 3.4 million were diagnosed with COVID-19 for the first time. Subsequent periods could not be analyzed due to insufficient testing.
This approach does have its limitations. For instance, the data does not indicate whether children who experienced these complications made a full recovery, and many mild COVID-19 cases amongst children may not have been formally recognized. “However, despite these constraints, the scale of the data and the comprehensive connection across all NHS data instills great confidence in our overall conclusions today,” says Wood.
“It’s crucial to understand that findings relevant to the strain of the coronavirus prevalent during the peak of the pandemic may differ for the current strain,” advises William Whiteley from the University of Edinburgh, UK, who was not involved in the study. His team previously reported that COVID-19 vaccines reduce the risk of heart attacks and strokes for at least six months post-vaccination.
The fact that nearly all individuals, apart from very young children, now possess some level of immunity to COVID-19 means they may respond differently to both booster shots and reinfections, according to team members including Peer Hardelid from University College London. “Ongoing research is essential,” she emphasizes.
Gentle exercises, like walking, can enhance brain health
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Older adults, particularly those at greater risk for Alzheimer’s disease, might slow cognitive decline by walking just 3,000 steps daily. The underlying reasons for this effect remain unclear; however, it could be linked to how regular exercise influences inflammation and blood circulation in the brain.
Earlier studies connecting regular physical activity to reduced cognitive decline often depended on individuals recalling their activity levels, with limited exploration into why staying active might offer such benefits.
To overcome these constraints, Wai Ying Wendy Yau and colleagues at Harvard University objectively tracked the physical activity of 296 cognitively healthy adults aged 50 to 90 through step-counting devices over a week.
Most participants also underwent brain imaging to assess baseline levels of misfolded proteins known as tau and beta-amyloid, which are believed to contribute to Alzheimer’s disease. These levels were typically evaluated every 2 to 3 years over a follow-up duration spanning 3 to 14 years. Participants took annual cognitive tests measuring memory and processing speed.
The research team estimated exercise’s impact on cognitive decline by feeding data from step counts, brain imaging, and cognitive evaluations into a statistical model. They discovered that participants with elevated levels of misfolded beta-amyloid who walked between 3,000 to 5,000 steps daily considerably slowed tau accumulation, but not beta-amyloid.
“[Exercise is] somehow hindering the spread of tau protein, which is more closely linked to symptom onset in individuals with [Alzheimer’s disease] than amyloid beta,” remarked Charles Marshall at Queen Mary University of London.
This was associated with an approximate 40 percent reduction in cognitive decline over a nine-year average follow-up, compared to participants taking fewer than 3,000 steps daily, categorized as inactive. Researchers, however, did not have data on whether any participants were diagnosed with Alzheimer’s during the follow-up.
Conversely, walking between 5,000 and 7,500 steps daily further slowed tau buildup, leading to a 54 percent reduction in cognitive decline compared to inactivity. However, exceeding 7,500 steps daily did not result in additional cognitive improvements. “The benefits with tau and cognition eventually reach a plateau,” Yau noted.
While the exact mechanisms through which regular exercise yields these effects remain uninvestigated, potential causes may include: Physical activity that diminishes inflammation purportedly caused by beta-amyloid and tau misfolding, disrupting neural connections, and damaging cells. Moreover, exercise could enhance blood flow or boost levels of protective hormones in the brain.
Nonetheless, this study does not conclusively establish that walking 5,000 steps daily directly contributes to slowing cognitive decline. Unidentified or unnoticed pre-existing conditions might impact individuals’ capacity and enthusiasm for exercising, according to Marshall. Various lifestyle and socio-economic factors that the research team considered may also affect activity levels and tau counts.
Nevertheless, given that regular exercise offers numerous health advantages, is inexpensive, and generally has few side effects, individuals should be encouraged to aim for at least 3,000 steps daily, even if the exact impact on cognitive function remains uncertain. “I always advise people not to obsess over numeric goals for step counts. It’s merely a target,” said Marshall. “What truly matters is maintaining regular physical activity, which doesn’t have to be at large volumes or high intensity.”
Prior research suggests that consistent lifestyle alterations, including exercise, can reverse cognitive decline. However, Yau emphasizes the necessity for further studies that randomly assign participants to distinct daily step counts to differentiate the effects of exercise from other lifestyle modifications and determine whether it genuinely slows tau accumulation.
Inquiring about the health advantages of living near a golf course might come off as someone attempting to leverage scientific studies to persuade their partner that residing adjacent to Gleneagles is a wise choice.
Fair play. I genuinely respect this transparent application of science. So, here’s some evidence from the archives.
When you tee off, appreciate all that lush greenery. Research consistently indicates that residing near green spaces correlates with a diminished risk of conditions such as cardiovascular disease and obesity.
While quantifying these effects is challenging, the study suggests it might lower stress hormones, enhance exercise, and benefit cognitive functions like memory and attention.
In one investigation, researchers concluded that a 10 percent increase in access to green and blue spaces resulted in a 7 percent decrease in anxiety and depression risk.
It’s well recognized that playing golf offers health benefits. In 2023, a Finnish study compared the cardiovascular impacts of playing an 18-hole round of golf (walking – no cart) to one hour of brisk walking and one hour of Nordic walking.
All three activities were beneficial, but golf proved to be the most effective, reducing blood pressure, cholesterol, and blood sugar levels.
Additional research has shown that golf training can provide cognitive benefits, particularly for older adults. It’s also advantageous for mental health due to its focus on fostering social connections.
In summary, regular golfing contributes to a longer and healthier life. Researchers found that individuals who played golf consistently experienced a 40 percent reduction in mortality.
That’s not a bad score, but there are some hazards to be aware of. At the start of 2025, a study explored the possible link between Parkinson’s disease and proximity to golf courses, highlighting potential exposure to pesticides.
Some chemicals used to maintain greens and fairways are neurotoxic, and numerous studies have associated them with Parkinson’s disease (although the risks are influenced by factors such as the type of pesticide and level of exposure).
Chemicals used on golf courses to maintain grass health may contribute to Parkinson’s risk – Credit: David Madison via Getty
In recent studies, researchers surveyed residents living near 139 golf courses in the United States. They discovered that individuals living within one mile of a golf course faced a 126 percent higher likelihood of developing Parkinson’s disease compared to those more than 6 miles away.
The risk nearly doubled for those sharing the same water supply zone as a golf course, suggesting that groundwater contaminated with pesticides, along with airborne transmission, may also play a role.
It’s crucial to note that the risk of Parkinson’s disease arises from a complex interplay of genetic and environmental factors. Risks associated with these chemicals are predominantly linked to occupational exposure rather than recreational exposure.
If you happen to reside in the UK, your risk might be lower, as paraquat, a chemical linked to Parkinson’s disease, is prohibited.
Thus, living next to a golf course presents a multifaceted situation, much like residing anywhere else. Why not head to the 19th hole and ponder this?
This article (by Carlisle native Paul Leach) addresses the question: “Will I be healthier if I move next to a golf course?”
If you have any inquiries, feel free to email us at:questions@sciencefocus.com or send us a messagefacebook,×orInstagramPage (please include your name and location).
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The oral microbiome extracted from King Richard III, derived from analysis of his dental plaque, indicates he may have suffered from a condition that could lead to jaw deterioration.
In 2012, the skeletal remains of Richard III were found beneath a parking lot at the former Greyfriars Church in Leicester, England. Initially thought to be Richard III—who was killed in the Battle of Bosworth Field in 1485 and interred in Leicester—dental and skeletal evidence, including a head wound and spinal curvature, correlated with descriptions from his death. Subsequent genetic tests confirmed the identity of the remains.
Although Richard’s reign only lasted two years amid the Wars of the Roses, he significantly impacted English history, with allegations of plotting against his nephews while they were imprisoned in the Tower of London, alongside William Shakespeare’s portrayal of him as a malevolent figure in his famous play.
Nevertheless, details of Richard’s daily existence are scarce. To uncover more, Turi King and fellow researchers at the University of Bath, UK, collected samples of tartar—hardened dental plaque—from three of his well-preserved teeth.
Dental plaque is effectively a time capsule, retaining DNA from microorganisms and remnants of food. “The quantity of DNA obtained from Richard III’s tartar is among the highest recorded in archaeological contexts,” the researchers stated, noting the detection of over 400 million DNA sequences.
“No one has previously sequenced 400 million ancient DNA fragments; it’s an astonishing figure,” remarks Laura Weyrich from Pennsylvania State University. “This indicates that our capabilities with ancient DNA are likely more extensive than previously thought.”
Dr. King and his team identified almost 400 microbial species from the DNA, comparable in variety to samples from well-preserved dental tartar across Britain, Ireland, Germany, and the Netherlands over the last 7,000 years, spanning from the Neolithic to modern times. “It suggests that elite populations shared microbial strains akin to those of the broader populace, despite their affluent lifestyles and experiences,” Weyrich notes.
However, the research team could not collect adequate plant or animal DNA to determine Richard’s dietary habits. Nevertheless, previous studies on his bones from his last two years indicated he drank non-local wine and consumed large quantities of game, fish, and birds, including swans and herons.
Professor Weyrich indicated that results regarding the microbiome could vary if the team obtained samples from more than one tooth and compared them to similar teeth from groups in Germany or the Netherlands. She also mentioned that their limited sampling does not provide a comprehensive view of Richard’s oral microbiome, as distinct bacteria inhabit different areas of the mouth and different surfaces of the teeth.
The king’s well-preserved teeth may provide insights into his oral microbiome.
Carl Vivian/University of Leicester
One particularly prevalent bacterium identified is Tannerella forsythia, which is linked to periodontal disease, a serious gum infection that can lead to bone loss around the teeth. Given the poor oral hygiene of the 15th century, Richard had a cavity when he died at age 32, though this does not automatically indicate he had periodontal disease.
“Many individuals may harbor potentially harmful bacteria without becoming ill, while others could become infected,” explains Pierre Stollforth from the Leibniz Institute for Natural Products Research and Infection Biology in Germany. Weyrich adds that examining bone loss in the jaw could reveal if Richard suffered from periodontal disease.
“I’m particularly passionate about bridging social science, history, and genetics,” Stallforth states. “Having access to the dental tartar of historical figures is extraordinary as it enables us to gain deeper insights into their lives.”
Parkinson’s disease is currently the fastest-growing neurological disorder in the United States; currently, 90,000 individuals have been diagnosed—a staggering 50% increase since the mid-1980s. The situation mirrors global trends, with an expected 25 million diagnoses by 2050, effectively doubled compared to today’s figures.
In summary, this is a significant issue. However, these numbers aren’t entirely surprising, considering longer life spans and growing populations. What is truly alarming, and frankly, unsettling, is how unprepared we are for this impending wave.
The available treatments are limited. Diagnostic tools are inadequate. Honestly, we still don’t really understand what causes Parkinson’s disease.
Yet, before you plunge into the depths of neurodegenerative despair, there is hope. Scientists worldwide are actively working to change the narrative surrounding Parkinson’s.
In particular, researchers are revolutionizing how we can detect Parkinson’s disease. Armed with cutting-edge technologies, AI, and a fundamentally evolving understanding of disease manifestation throughout the body, they’re aiming to detect it decades before any symptoms present themselves, rather than years.
Presently, there is no single definitive test for Parkinson’s disease. Instead, doctors diagnose it based on physical symptoms like tremors, slow movement, and muscle stiffness, often requiring assessments of tasks such as writing and speaking.
“Today’s neurodegenerative disease is what cancer used to be 50 years ago,” states Professor Hermona Solek, a leading researcher in next-generation diagnostic tools. “We often finalize a diagnosis only when all involved nerve cells are already dead, leaving us unable to properly treat the patient.”
But what if there were a way to diagnose Parkinson’s disease before it could do any significant harm? What if it could be caught on its way, before brain cells face irreversible damage?
This is no longer just a theory. In fact, there are multiple methods emerging.
AI Desk Accessories
Not all breakthroughs in diagnostics require a blood sample; some new innovations could be found right on your desk.
At the University of California, Los Angeles, Professor Junchen‘s lab claims to have developed a diagnostic pen that detects Parkinson’s disease by analyzing your writing.
This unique pen’s soft tip is crafted from an innovative magnetoelastic material that alters the magnetic field in response to pressure or bending—a phenomenon previously known in rigid metals but now applied to soft polymers, creating a new type of highly sensitive and user-friendly sensor.
“Utilizing magnetoelastic effects with soft materials represents a new operational mechanism,” Chen explains. “It can translate small biomechanical pressures, like arterial vibrations, into high-fidelity electrical signals.”
The pen, filled with magnetized ink, captures movements occurring both on paper and in the air, subsequently sending this data to a computer. Here, AI models analyze specific patterns linked to Parkinson’s motor symptoms.
Smart pens can be especially beneficial in countries where affordable diagnostic tools are needed—UCLA Jun Chen Lab
In a pilot study, the system successfully distinguished individuals with Parkinson’s disease from healthy controls with over 96% accuracy. Even better, Chen believes this pen can be mass-produced for merely $5 (£3.70).
“We have already filed for a patent and aim to commercialize this pen,” Chen states. “Simultaneously, we are working on optimizing it to improve our diagnostics’ accuracy.”
If handwriting isn’t your preferred method, Chen’s team has you covered. They’ve also created a Smart Keyboard utilizing the same principles.
This keyboard tracks subtle changes in pressure and rhythm as users type—often imperceptible to the naked eye—and relays that information to machine learning algorithms.
Initial tests indicate that it can identify characteristic motor abnormalities in Parkinson’s disease, and the team is combining this technology with a mobile app for continuous remote monitoring.
Together, these intelligent desk tools offer a glimpse into what Chen describes as the “personalized, predictive, preventive, participatory” future of Parkinson’s healthcare; a future where diagnosis is as simple as taking notes or sending emails.
This portable, soft keyboard employs magnetic elasticity to detect Parkinson’s disease and sends results to your smartphone—UCLA Jun Chen Lab
Parkinson’s Eye Test Detects Changes Two Decades in Advance
Picture diagnosing Parkinson’s disease during a routine eye exam, potentially decades before symptoms manifest. This is the promise of new non-invasive techniques developed by Victoria Soto Linan and her colleague at Laval University in Canada, using an established eye test known as electroretinography (ERG).
According to Soto Linan, this eye test serves as a “window to the brain,” as it’s part of the central nervous system. Issues like blurred vision and diminished contrast sensitivity manifest long before the well-known symptoms of tremors and stiffness.
The Soto Linan team collected data on how the retina responds to light flashes from both mice engineered to develop Parkinson-like symptoms and newly diagnosed human patients.
They identified unique retinal signals demonstrating “sick signatures,” particularly in women. Crucially, this weakened signal appeared in the mice prior to any behavioral disease signs.
This leads Soto Linan to believe that this eye test could detect Parkinson’s as much as 20 years before symptoms arise.
Read more:
And unlike other early diagnostic methods, this one is already well ahead of the game.
“ERGs are now employed in clinics to diagnose eye diseases,” she explains. “They also have the major advantage of being non-invasive.”
The patient sits before a dome that flashes lights, capturing how the retina responds. This could easily be integrated into a few minutes of your annual vision test.
The team is currently focusing on enhancing the testing process, with hopes of linking it to machine learning algorithms that will accelerate results, perhaps even making them portable to smartphones.
While the research is still in its early stages, its potential ramifications are enormous. As Soto Linan states, “This tool could identify at-risk individuals up to 20 years before symptoms emerge. Imagine how much less damage could be done by then.”
“Even if there is no treatment available, early intervention can often improve the quality of life in the long run.”
Detecting Parkinson’s Through Vocal Patterns
Can your voice indicate Parkinson’s disease before your physical body does? Recently, preprint research has explored whether AI can identify Parkinson’s simply by analyzing a person’s speech.
Around 90% of individuals with Parkinson’s develop motor speech disorders known as dysarthria, which can lead to issues like irregular pitch and breath control.
Globally, over 8.5 million individuals live with Parkinson’s disease—Getty
These vocal changes often arise earlier than more noticeable motor symptoms like tremors, thus serving as promising early indicators.
The research team collected brief audio recordings from 31 to 195 individuals, which included 33 individuals with the disease. Their data served to train four different AI models to recognize disease-related vocal patterns. When tested on new recordings from the same participants, the models identified Parkinson’s with an accuracy exceeding 90%.
These changes are subtle and occur early, and researchers suggest that speech-based assessments could provide low-cost, non-invasive diagnostic options.
Blood Tests for Diagnosing Parkinson’s
In April 2025, SOREQ and her colleagues—including her son—announced a groundbreaking new study.
The findings were surprising; they revealed a simple and inexpensive blood test utilizing PCR technology (remember this from COVID-19?) that can accurately detect Parkinson’s disease a few years prior to symptom onset.
This test functions by measuring the ratio between two markers that SOREQ and her team discovered in human blood.
Specifically, individuals with Parkinson’s exhibit abnormally high levels of certain molecules known as transfer RNA (tRNA) fragments, identifiable by a specific repeating pattern called conserved sequence motifs.
A new blood test can detect early Parkinson’s by analyzing the unique imbalance of small RNA molecules in your blood—Credit: Getty
Simultaneously, the team uncovered reduced levels of tRNA associated with mitochondria (the “powerhouses” of cells, responsible for producing most of your body’s energy) in the blood of Parkinson’s patients.
“We proposed that if there’s an increase in one sequence and a decrease in another, we could calculate the ratio and identify a probable diagnosis,” says Soreq.
If this ratio exceeds a specific threshold, it strongly indicates a diagnosis.
According to SOREQ, a traditional diagnosis of Parkinson’s can cost up to $6,000 (£4,400). The two PCR tests required for their method? Only $80 (£60).
“This is monumental. It makes a substantial difference,” she states. With some luck, the team anticipates this will become widely available within the next decade, potentially providing a crucial lifeline for patients globally.
For the first time, researchers have successfully visualized and quantified small protein clusters in the human brain that may signal the onset of Parkinson’s disease.
These clusters, known as alpha-synuclein oligomers, have long been implicated in some of the fastest-expanding neurological disorders worldwide but had never been observed in brain tissue until now.
To identify these elusive proteins, the research team utilized a novel imaging method called Advanced Sensing of Parkinson’s Disease (ASA-PD) aggregates, which renders these nanometer-scale (one billionth of a meter) oligomers visible.
For decades, clinicians could confirm a diagnosis of Parkinson’s disease only by detecting larger deposits of proteins that build up in neurons. However, many researchers believe the disease actually initiates with these smaller oligomers.
“You can think of Lewy bodies as a sort of morbid gravestone,” stated Professor Stephen Lee from Cambridge’s Yusuf Hameed Department of Chemistry, who co-led the study. BBC Science Focus. “They indicate where the disease resides and its progression.”
To investigate the earlier phases of the disease, the team compared post-mortem brain samples from individuals with Parkinson’s disease to those from healthy individuals. Oligomers were present in both cohorts, surprising scientists, but were more abundant and vibrant in the brains of Parkinson’s patients.
“This marks the first occasion we’ve directly observed oligomers in human brain tissue at this scale, akin to spotting stars in daylight,” commented Dr. Rebecca Andrews, Co-First Author and former postdoctoral researcher in Lee’s lab.
The researchers also discovered subtle variations in the distribution of oligomers, which could signify the earliest stages of the disease prior to the onset of symptoms.
Scientists were able to visualize and count α-synuclein oligomers (shown in red) in brain tissue samples. Interestingly, these puncta were present in both Parkinson’s patients and healthy individuals, as depicted in the images of two Parkinson’s patients (top) and two healthy controls (bottom) – credits: Andrews et al. (2025)
Lee emphasized that while this study is a significant advancement, it should not be misconstrued as a means to directly find treatments. “We’re not at that stage,” he noted. “This research actually allows us to engage with the very early stages of the disease. From a therapeutic standpoint, it lays the groundwork for future developments.”
Currently, over 10 million people globally suffer from Parkinson’s disease, which lacks a treatment that addresses the underlying condition. Existing medications can manage symptoms like tremors, but none target the disease’s root cause or halt its progression.
A collaborative team from the University of Cambridge, the University of London, the Francis Crick Institute, and Polytechnique Montreal aims to utilize these findings to enhance methods for monitoring the efficacy of diagnostic tests and experimental treatments.
This imaging technique is also applicable beyond just Parkinson’s disease. “This approach provides more than just a snapshot,” said Professor Lucian Weiss from Polytechnique Montréal, who co-led the study. “It maps protein changes throughout the brain and similar techniques can be applied to other neurodegenerative disorders such as Alzheimer’s and Huntington’s diseases.”
“Oligomers were once like needles in a haystack, and now that we know their precise locations, it enables us to target specific cell types in designated areas of the brain.”
The caudate nucleus is one of the brain regions that gene therapy targets
Kateryna Kon/Science Photo Library
Innovative gene therapy has emerged as the pioneering treatment that effectively slows the progression of Huntington’s disease. While the results are still in their early stages, this method holds significant promise and could even pave the way for new therapies for other neurodegenerative disorders, including Parkinson’s and Alzheimer’s diseases.
How does the treatment function?
The therapy known as AMT-130 specifically targets the abnormal brain proteins associated with Huntington’s disease progression. Those affected by the condition possess genetic mutations that result in the accumulation of huntingtin proteins, which form toxic aggregates in brain cells, leading to cell death. This eventually manifests as memory loss, mobility issues, speech impairment, and various other symptoms.
Therapies from the Dutch biopharmaceutical company Uniqure aim to halt the production of these mutant proteins. The process involves delivering genetic material to brain cells using a harmless virus. This genetic material instructs the cells to produce small RNA molecules called microRNAs that effectively block and eliminate the signals that lead to the generation of toxic proteins. It acts similarly to a molecular stop signal.
Procedures and Location of Treatment
This therapy initially focuses on two specific brain areas impacted by Huntington’s disease: the caudate nucleus and the putamen. These regions are located deep within the brain, requiring doctors to utilize real-time brain imaging to navigate thin catheters into place. The entire procedure duration ranges from 12 to 18 hours, and preliminary results suggest that a single injection may be adequate to permanently reduce levels of mutant huntingtin in the brain.
What is the efficacy of gene therapy?
Initial findings released by Uniqure indicate that gene therapy may slow the advancement of Huntington’s disease by approximately 75%.
The revelation stems from a clinical trial spearheaded by Sarah Tabrizi of University College London, where 17 Huntington patients received high-dose treatment. After three years, researchers noted the deterioration in cognitive function, motor skills, and daily activities compared to a similar group of untreated individuals. Tabrizi remarked that the decline typically observed over a year in untreated patients was instead noted within four years for those receiving treatment. BBC News. Additionally, those treated exhibited reduced levels of proteins associated with brain damage in their cerebrospinal fluid, highlighting the potential of gene therapy in slowing Huntington’s progression.
“These findings reaffirm our conviction that AMT-130 could revolutionize the treatment landscape for Huntington’s disease,” stated Walid Abi-Saad from Uniqure in a press release.
Are there any side effects?
While Uniqure has not provided comprehensive data on the side effects of the treatment, initial reports suggest that the drug appears to be safe and well-tolerated. The most frequently reported side effects included headaches and confusion, which generally resolved with steroid treatment to reduce inflammation.
When will the treatment be accessible?
In a recent press announcement, Uniqure indicated that it anticipates submitting an application to the U.S. Food and Drug Administration early next year, with the potential for product availability as soon as before 2027 with expedited approval.
“However, it is still in the preliminary phase, and further testing is necessary to assess the long-term effects of this new gene therapy and any potential side effects,” noted Zofia Miedzybrodzka from the University of Aberdeen, UK, in a statement.
Could this method assist in treating other brain disorders?
If successful, the gene therapy could facilitate the development of analogous treatments for various neurodegenerative diseases, including Parkinson’s and other forms of dementia, according to David Rubinsztein from Cambridge University. Researchers could manipulate genetic material to target the toxic proteins that cause these conditions. “This could represent a significant breakthrough,” he remarked.
A recent proof-of-concept study conducted by researchers at Lund University reveals that a brief self-management digital cognitive assessment called BioCog effectively detects cognitive impairments. When used alongside blood tests, it can accurately identify clinical Alzheimer’s disease in primary care settings.
In primary care, the BioCog test achieved 85% accuracy in identifying cognitive impairments with a single cutoff, significantly outperforming primary care physicians, who had a 73% accuracy rate. Image credit: Miroslaw Miras.
Alzheimer’s disease stands as the leading cause of dementia, marked by amyloid beta accumulation, tau aggregation, and progressive neurodegeneration.
Clinical presentations of Alzheimer’s typically begin with subjective cognitive decline, where individuals report memory issues and other cognitive challenges, although formal cognitive tests may not yet indicate impairment.
This initial phase advances to mild cognitive impairment, which is characterized by objective cognitive symptoms, ultimately evolving into dementia marked by significant functional limitations in daily life.
Diagnosing Alzheimer’s in its early stages, especially in primary care, can be particularly challenging.
There’s a considerable prevalence of both misdiagnosis and missed diagnoses, with 20-30% of cases incorrectly diagnosed in specialist environments and about 40% in general practice when Alzheimer’s is not corroborated by biomarkers.
“The BioCog digital assessment, designed to allow patients to perform with minimal healthcare worker involvement, will enhance primary care physicians’ ability to investigate potential Alzheimer’s pathology early through blood tests,” stated the researchers.
“Primary care typically lacks the resources, time, or expertise to explore Alzheimer’s disease with the same thoroughness as specialized memory clinics.”
“This is where digital cognitive assessments can play a vital role.”
In contrast to the traditional pen-and-paper tests utilized for evaluating cognitive impairment, digital assessments offer a more comprehensive analysis.
They easily integrate novel variables and additional factors that were not previously measured.
“Most individuals experiencing memory loss first seek help at their local health center,” remarked Pontus Tideman, a doctoral student at the University of Rand and psychologist at Skone University Hospital’s memory clinic.
“Our new digital evaluations provide the initial objective insights needed, ensuring higher accuracy in identifying cognitive impairments related to Alzheimer’s disease.”
“This determines who should undergo a blood test that measures phosphorylated tau levels, which can reliably detect Alzheimer’s disease in the brain.”
Currently, these blood tests are available exclusively at hospital specialty and memory clinics.
In time, they are expected to be accessible in primary care; however, it is not intended for all patients with cognitive complaints to undergo blood testing.
Researchers assert the immense value of digital solutions, given the challenges of diagnosing Alzheimer’s during a typical 15-20 minute patient consultation.
This is where objective digital tools for assessing cognitive skills can significantly alter the diagnostic landscape.
“A distinctive feature of our BioCog assessments is their validation within primary care settings, unlike many other digital evaluations. These assessments are aimed at patients seeking treatment due to cognitive concerns, such as memory problems,” the researchers noted.
“The combination of digital assessments with blood test results can greatly enhance the diagnostic accuracy of Alzheimer’s disease.”
“The goal of this test is to simplify the process for primary care physicians.”
The BioCog test is detailed in a study published in the journal Nature Medicine.
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P. Tideman et al. Primary care detection of Alzheimer’s disease using self-administered digital cognitive tests and blood biomarkers. Nat Med. Published online on September 15th, 2025. doi:10.1038/s41591-025-03965-4
Recent studies indicate that the link between different lipids and Alzheimer’s disease is particularly significant for women, often absent in men.
wretlind et al. The research focuses on gender-specific lipids associated with Alzheimer’s disease. Image credit: Wretlind et al, doi: 10.1002/alz.70512.
Alzheimer’s disease (AD) is a severe neurodegenerative condition that is increasingly impacting people globally.
Women experience a disproportionate prevalence of AD, comprising about two-thirds of all diagnosed cases.
“Women face a higher risk of AD and are often diagnosed with the condition more frequently than men post-80 years of age,” stated Dr. Christina Legidokigley, a researcher at King’s College London.
“One of the most striking findings I noticed when examining gender differences was that healthy men and those perceived as healthy did not show variations in these lipids, whereas the situation was markedly different for women.”
“This study highlights that lipid biology in AD varies by gender and opens new avenues for investigation.”
The researchers analyzed plasma samples from 841 individuals with AD, mild cognitive impairment, and those in cognitive health, measuring brain inflammation and damage.
Utilizing mass spectrometry, they examined 700 distinct lipids in the bloodstream. Lipids comprise a diverse group of molecules.
Saturated lipids are typically deemed “unhealthy,” in contrast to unsaturated lipids that contain omega fatty acids, which are often labeled as “healthy.”
Researchers observed a substantial increase in saturated lipids among women diagnosed with Alzheimer’s compared to those in the healthy group—deemed “unhealthy lipids.”
Conversely, lipids with omega fatty acids were found to be significantly diminished in those with Alzheimer’s.
“Our findings suggest that women should ensure they are incorporating omega fatty acids into their diets.”
“However, clinical trials are crucial to determine whether changes in lipid composition can influence the biological progression of AD.”
“It has been known for some time that more women than men are diagnosed with AD,” remarks Dr. Asgaretlin, also from King’s College London.
“This remains an area for further exploration, but we managed to identify biological differences in lipids across genders in extensive cohorts and underline the significance of omega-containing lipids in the blood, which has not been previously demonstrated.”
“The results are quite striking, illustrating how these changes manifest early in life among women.”
This study was published today in Alzheimer’s Disease and Dementia: Journal of the Alzheimer’s Disease Association.
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Asger Wretlind et al. 2025. Lipid profiling uncovers reductions in unsaturated lipids among women with Alzheimer’s disease. Alzheimer’s Disease and Dementia 21(8): E70512; doi: 10.1002/alz.70512
Human Y (right) and X chromosomes observed with scanning electron microscopy
Power and Syred/Science Photo Library
A recent study involving over 30,000 individuals has revealed that men who experience a loss of Y chromosomes in a substantial number of immune cells are at a higher risk for narrower blood vessels, a significant factor in the development of heart disease.
“The loss of Y chromosomes greatly impacts men,” states Kenneth Walsh from the University of Virginia, who was not involved in the research. “Men’s lifespan averages six years shorter than women’s, primarily due to the instability of sex chromosomes.”
Loss of the Y chromosome is one of the most prevalent mutations following conception in men. This phenomenon typically occurs in leukocytes, the immune cells responsible for attacking and eliminating pathogens, as the rapidly multiplying stem cells that generate white blood cells undergo division. The cells without Y chromosomes accumulate and become more frequent as individuals age; approximately 40% of 70-year-old men show detectable losses.
This issue gained traction in 2014 when Lars Forsberg from Uppsala University in Sweden and his colleagues noted that elderly men with significant Y chromosome loss in their blood typically had a lifespan that was five years shorter than those without it. Walsh later linked this loss to heart disease.
Forsberg and his research team have now uncovered further connections between Y chromosome loss and specific cardiovascular issues. They analyzed data from Swedish cardiopulmonary bioimaging studies, which provided detailed vascular scans of 30,150 volunteers aged between 65 and 64. None of the participants exhibited symptoms of cardiovascular disease; however, they were assessed for vascular stenosis or atherosclerosis.
Among the male participants, 12,400 possessed the necessary genetic information to evaluate their Y chromosome loss. They were categorized into three groups: those with no detectable Y loss in leukocytes, those with less than 10% loss, and those with over 10% loss. Atherosclerosis scores for these groups were then compared with each other and with a female cohort in the study.
The researchers discovered that approximately 75% of men who had the highest Y chromosome loss exhibited narrowed blood vessels, while around 60% of those with less than 10% loss showed similar findings.
Despite some atherosclerosis being observed even in those with undetectable Y loss, about 55% of men and roughly 30% of women in this category had been affected. “Clearly,” Forsberg noted, “[loss of Y] involves other factors.”
In the coming months, Thimoteus Speer and colleagues from the University of Goethe in Frankfurt studied men undergoing angiography, an X-ray technique for examining blood vessels due to suspected cardiovascular disease. They found that over the next decade, individuals who lost Y chromosomes in more than 17% of their immune cells were more than twice as likely to die from a heart attack compared to those with less affected cells.
“The findings of Lars Forsberg and our study are quite consistent,” Speer remarked. “He observes increased coronary atherosclerosis, correlating it with a higher risk of mortality from myocardial infarction [heart attack], emphasizing the relationship with coronary atherosclerosis.”
Walsh acknowledges that neither study definitively proves that Y chromosome loss directly causes these outcomes. However, statistical analyses suggest its independent effect aside from smoking or aging— the primary risk factors for mutations.
The pressing question remains: how does Y chromosome loss impact health? Previous research by Walsh indicated that removing chromosomes from mouse immune cells adversely affects the cardiovascular system by driving fibrosis, which is the formation of scar tissue. However, heart attacks and atherosclerosis are typically more associated with inflammation and lipid metabolism defects than fibrosis. Both Speer and Walsh assert that more research is essential to unravel this relationship.
With a deeper understanding of the underlying processes, Speer hopes that future blood tests for Y chromosome loss will guide proactive interventions. “[These tests] may help in identifying patients who could particularly benefit from specific treatments,” he concludes.
Exposure to light at night significantly raises the risk of heart disease, according to extensive research.
Various environmental and behavioral signals synchronize the body’s circadian rhythms, the internal clocks that manage physiological functions. However, contemporary lifestyles often disrupt these biological mechanisms, heightening sensitivity to health issues.
Previous studies utilizing satellite data have indicated associations between residents of brightly lit urban areas and heart disease, focusing solely on outdoor light at night. Daniel Windred, from Flinders University in Adelaide, and his team sought to determine if overall light exposure impacts cardiovascular health.
They monitored approximately 89,000 individuals without pre-existing cardiovascular conditions, equipping them with light sensors for a week between 2013 and 2016. “This represents the largest research effort on personal light exposure patterns affecting cardiovascular health to date.”
The sensors captured both natural and artificial light sources, including emissions from mobile phones. Over the eight-year period, participants who experienced the brightest nights showed a 23-56% increased risk of developing cardiovascular disease compared to those exposed to darker nights.
For example, individuals in the highest light exposure category included those who activated overhead lights for an hour from midnight to 6 AM. “This scenario places them within the 90th to 100th percentiles of nighttime light exposure,” Windred noted. He emphasized that the body continues to react to artificial light even after it is turned off, and short exposures can disrupt circadian rhythms.
Researchers accounted for factors such as gender, age, smoking habits, and shift work. They also demonstrated that the connection between light exposure and heart disease risk remained constant, regardless of sleep duration, sleep efficiency, or genetic predisposition.
Interestingly, although women generally have a lower incidence of heart disease at the same age as men, exposure to bright nighttime light can neutralize this protective effect due to estrogen. Evidence suggests that women experience more significant melatonin suppression in response to bright light, making their circadian systems more sensitive compared to men.
Disruption of circadian rhythms can compromise glucose tolerance, elevating the risk for type 2 diabetes, which is a risk factor for heart disease. Such disruption also influences blood pressure and can increase the risk for abnormal cardiac rhythms due to conflicting signals between the brain and heart.
“The significance of these findings must not be understated,” stated Martin Young from the University of Alabama at Birmingham. “As a 24/7 society increasingly disrupts our circadian systems, this study underscores the notable health risks linked to such exposure.”
Windred suggests that individuals strive to maintain a darker nighttime environment. “Optimize your sleep schedule to ensure darkness during bedtime. If you awaken during the night, utilize dim lighting and avoid bright overhead lights.”
Kidney disease can result in hypertension and infections
Mohammed Haneefa Nizamudeen/Getty Images
Recent animal research suggests that damage caused by the most prevalent hereditary kidney disease may not be as irreversible as previously thought. Researchers are using CRISPR gene editing to potentially reverse certain mutations responsible for the condition.
Polycystic kidney disease (PKD) gradually alters kidney function, leading to debilitating effects. “It was generally believed that correcting the mutations would not change the outcome,” says Michael Kaminski from Berlin University of Medicine.
PKD results in the formation of fluid-filled cysts in the kidneys and liver, leading to organ failure and necessitating dialysis or transplants. Besides organ failure, damage and swelling can lead to other severe issues, including high blood pressure and infections.
The disease typically affects adults, with approximately 12 million individuals globally estimated to be affected. Symptoms may not manifest until the cysts reach significant size in one’s 30s, by which point there may already be extensive damage to the kidneys and liver.
Kaminski’s team has utilized a CRISPR method known as base editing to correct mutations in the PKD1 gene in mice models.
This technique successfully corrected mutations primarily in the liver, resulting in a reduction in both the size and number of cysts post-treatment. Kaminski noted potential improvements in the kidneys as well.
Specifically, Xiaogang Li’s team at Mayo Clinic conducted a similar study using more precise methods targeting the kidneys, indicating a reduction in cyst size and quantity, according to Li.
Both teams employed viral vectors to deliver gene-editing tools, which poses challenges with repeated doses due to immune responses might hinder treatment. “This is a legitimate concern,” Li notes. “However, we’ve observed limited immune responses in our animal models so far.”
Utilizing lipid nanoparticles instead of viral vectors, as seen in mRNA vaccines, could mitigate immune-related issues, but Kaminski warns that these particles may struggle to penetrate deeply into the kidneys through the bloodstream. “I believe that the delivery method using [lipid nanoparticles] might become more feasible through urinary pathways,” he says.
Another limitation is that base editing primarily addresses single-character mutations, rendering it ineffective for individuals with longer mutation sequences. However, Li reports successful outcomes using a technique known as Prime editing.
These findings are poised to be published shortly in scientific journals, with plans for human trials to follow. “After our publication, I aim to organize a small clinical trial,” he states.
The broader implications of this research suggest that if PKD can indeed be reversed, it could ignite more research into this potential therapeutic avenue. Currently, the only approved treatment is tolvaptan, which only slightly slows disease progression and requires significant fluid intake.
Baby KJ Rebecca Affles Nicklas and Kiran Musnul after gene editing injection with researchers
Philadelphia Children’s Hospital
A young boy afflicted with a serious genetic disorder is set to be the first recipient of personalized CRISPR gene editing treatments, offering a glimpse into the potential future of medicine.
This groundbreaking event marks the first instance of an individual receiving a gene editing therapy tailored to correct unique mutations contributing to their illness. Rebecca Ahrens-Nicklas explained during a press briefing held at Children’s Hospital in Philadelphia, Pennsylvania, “He is showing early signs of progress,” though she noted that it’s premature to determine the complete effectiveness of the treatment.
Researchers released information promptly, aiming to motivate others, as stated by team member Kiran Musnur at the University of Pennsylvania. “We sincerely hope that demonstrating the feasibility of personalized gene editing therapy for one patient within a few months will encourage additional efforts in this area,” he remarked.
“When I refer to this as the future of medicine, I believe I’m stating a fact,” he emphasized. “This is a crucial step towards employing gene editing therapies to address a range of rare genetic disorders that currently lack viable treatment options.”
KJ inherited mutations on both alleles of a liver enzyme gene known as CPS1. The absence of this enzyme leads to ammonia accumulating in the bloodstream, posing a risk of brain damage during the breakdown of dietary proteins. According to Ahrens-Nicklas, over half of children born with CPS1 deficiency do not survive.
She and Musnur are developing therapies targeting this condition by focusing on the liver, allowing them to rapidly formulate a basic editing therapy that modifies one of KJ’s two CPS1 gene copies.
The team engaged with US regulatory bodies early in the process. “They recognized the exceptional nature of this situation,” Musnur stated. “KJ was critically ill and time was of the essence. Following our official submission to the FDA [Food and Drug Administration] when KJ was six months old, we received approval within just a week.”
KJ underwent initial low-dose treatment at six months in February 2025, followed by higher doses in March and April. He is now able to consume more protein than before, albeit while still taking other medications for his condition.
Ideally, children should receive treatment earlier to mitigate long-term damages linked to conditions like CPS1 deficiency. As reported by New Scientist, Musnur has ambitions to enable gene editing in humans prior to birth one day.
In contrast, other gene editing therapies are designed for broader applications, aiming to work for many individuals irrespective of the specific mutations causing their condition. For instance, the first approved gene editing treatment for sickle cell disease functions by enhancing fetal hemoglobin production, rather than altering the mutations in adult hemoglobin responsible for the disorder. Despite being a “one-size-fits-all” solution, it comes at a price of £1,651,000 per treatment in the UK, as noted by Each treatment course costs £1,651,000.
KJ with his family after treatment
Philadelphia Children’s Hospital
Custom treatments can be significantly more costly. Musnur mentioned that he cannot provide exact figures for KJ’s treatment due to the extensive pro bono work by the involved companies. However, he is optimistic about a decline in costs. “As we enhance our methods, we can anticipate economies of scale, leading to a substantial reduction in prices,” he stated.
One barrier to the development of personalized gene editing therapies has been the regulatory perspective, which previously treated therapies targeting different mutations within the same gene as separate entities. This necessitated restarting the approval process for each mutation individually. However, there’s a growing movement towards a platform approach, allowing broader approvals for treatments targeting various mutations.
“Platform-based methods, like CRISPR gene editing, offer scalable solutions for even the rarest diseases, as exemplified by KJ’s case,” stated Nick Mead from Genetic Alliance UK, a charity that advocates for individuals with rare conditions. “This development finally renders treatment a plausible possibility for countless families.”
Six years ago, a Canadian neurologist noticed unusual symptoms among a group of patients in New Brunswick, a province next to Maine.
Dr. Arie Marrello reported that patients experienced hallucinations, convulsions, rapid memory loss, and a sensation of insects crawling under their skin, but these symptoms and brain scans didn’t align with existing diagnoses, making the cases puzzling.
Subsequent reviews by neurologists led to clear diagnoses, including Alzheimer’s disease, Parkinson’s disease, and cancer.
A recent study published in JAMA Neurology supports these findings, indicating that the likelihood of such mysterious illnesses is about one in one million.
The physicians involved in this study assessed 25 patients from the New Brunswick cluster. With 11 patients deceased, neuropathologists relied on autopsy findings to reach diagnoses. Among the 14 living patients, neurologists used cognitive assessments, concluding that all had well-documented conditions such as Alzheimer’s, Parkinson’s, cancer, traumatic brain injury, and post-concussion syndrome.
Dr. Anthony Lang, a neurologist at the Krembil Brain Institute within the University Health Network, remarked, “I was confident that there was a clear explanation for 100% of the cases.”
Nevertheless, some medical professionals are concerned that this evidence may not quell speculation about an underlying unknown cause, which many patients and their families continue to believe in.
According to the authors of the study, 52 individuals connected to the New Brunswick cluster declined a second opinion, and another 42 individuals were unreachable. This lack of response has been attributed to the spread of misinformation through both traditional and social media, undermining trust in healthcare systems.
“These instances reflect misdiagnosis, leading to misinformation. Unfortunately, the doctors involved persist in convincing patients and their families that they have a mysterious illness,” Lang emphasized.
Marello expressed skepticism regarding the study’s methods and conclusions in a statement, saying, “I hold serious reservations about the validity of the research and have numerous questions regarding its methodology and content. We believe that our patients, families, and communities share these significant concerns.”
Dr. Valerie Sim, an associate professor of neurology at the University of Alberta and not part of the study, stated there is no evidence linking the patients’ illnesses. She noted that the description of the cases is too broad and could apply to multiple conditions.
“Sadly, the unifying factor is that all these patients saw the same neurologist,” Sim pointed out. “Patients evaluated by different specialists have been diagnosed with known conditions that aren’t mysterious.”
James Mastorianni, a professor of neurology at the University of Chicago, highlighted that while not included in the study, it underscores the importance of seeking second opinions from experts in the field.
Ongoing Investigation
The Mystery Disease Theory gained traction in 2021 when Canadian health officials launched an investigation based on Marello’s observations. However, even after the inquiry determined that most patients had identifiable conditions, skepticism remained among families. In November, Susan Holt, the Prime Minister of New Brunswick, called for a scientific review of the “mysterious brain diseases.”
“The residents of New Brunswick deserve answers,” Holt stated in a public statement last year. “We must understand the source of our illnesses.”
Some advocates for patients suspect that environmental factors may be contributing to the illnesses, noting that blood tests have detected heavy metals, pesticides, and rare antibodies, warranting further investigation.
“None of our patients received an alternative diagnosis,” said Kat Lantine, an advocate in New Brunswick. “What led to their neurodegenerative disease?”
Dr. Yves Legger, New Brunswick’s chief medical officer of health, stated in a recent statement that the new study “does not alter our commitment to thoroughly investigating cases of undiagnosed neurological diseases in New Brunswick.”
His office has received 222 case reports in connection with this cluster.
Marello mentioned, “We have evaluated over 500 patients in this cluster and provided substantial evidence regarding environmental exposures, as well as rare autoimmune markers present in several cases.”
However, Lang cautioned that detecting substances in the blood or urine does not necessarily imply they are the cause of neurological symptoms.
“You cannot take a scattershot approach, where you find something and assert that it’s relevant to the health issue,” he explained.
Challenges in Diagnosing Neurological Problems
Neurologists not involved with the New Brunswick situation highlight several challenges that continue to spur discussions among advocates, doctors, and government officials about the illness’s origins.
For starters, they note that accurate diagnoses can take time. Some conditions highlighted in the study exhibit complex symptom profiles, like Alzheimer’s.
“We need a comprehensive history from the family along with a timeline to identify if someone is developing dementia. There may be early signs of confusion evident in neurological tests,” indicated Dr. Kimberly O’Neal, a neurologist at the Health Multiple Sclerosis Comprehensive Care Center at NYU Langone.
Rapidly progressing dementia was one of the key symptoms observed in New Brunswick patients. However, families sometimes overlooked early indicators of neurodegeneration, which made it appear as though dementia appeared suddenly, according to Mastorianni.
When severe symptoms manifest, patients and their families often seek answers and can be hesitant to abandon their initial diagnoses, Sim noted.
“This phenomenon is common in medicine. Patients often become attached to a diagnosis or a group of conditions,” Sim remarked. “That is evidently the case here.”
Misdiagnosis can be “truly tragic,” as it may prevent patients from receiving effective treatment and proper care.
Fatty liver disease can lead to cirrhosis and cancer
3dmedisphere/shutterstoc k
Currently, common medications used for treating obesity and diabetes are showing promise in combating life-threatening liver diseases.
Semaglutide, marketed under names like Ozempic and Wegovi, mimics the hormone GLP-1, which aids in weight loss and regulates blood sugar levels, helps suppress appetite, and promotes insulin secretion. Researchers have now found that this drug therapy can halt or even reverse a condition known as metabolic dysfunction-associated steatohepatitis (MASH).
“This could offer a groundbreaking way to manage this condition,” says Philip Newsom from King’s College London. “It’s incredibly promising for patients.”
MASH, formerly known as NASH, is a severe version of non-alcoholic fatty liver disease marked by inflammation, fibrosis (scar tissue formation), and excessive liver fat accumulation, occasionally leading to cirrhosis and cancer. MASH is commonly linked to obesity and often coexists with type 2 diabetes.
A study conducted in 2020 involving 320 participants revealed that daily semaglutide injections led to a reduction in liver fat and inflammation in 59% of those with MASH. However, a more recent investigation involving 71 patients found no benefits from the weekly dosage.
For a broader perspective, Newsom and Arun Sanyal from Virginia Commonwealth University initiated a larger trial involving 1,195 MASH patients across 253 clinical sites in 37 countries. Participants averaged 56 years old with a body mass index of 34.6, and about 50% had type 2 diabetes.
The physician prescribed each participant a weekly semaglutide injection for four and a half years, gradually increasing the dose to 2.4 milligrams over the first four months, mirroring those used in Wegovy based on prior test findings. Participants also received lifestyle counseling to encourage a healthier diet and exercise.
While the full study is ongoing, results from biopsies taken 72 weeks later revealed that among the first 800 patients, including 266 receiving a placebo, 62.9% of those on semaglutide showed significant reductions in liver fat and inflammation, compared to 34.3% in the placebo group. Improvements in fibrosis were observed in 36.8% of the treatment group versus only 22.4% for the placebo group. About one-third of all treated patients and 16.1% of placebo patients experienced these benefits.
Weight loss alone could explain some of these improvements, as patients in the treatment cohort lost an average of 10.5% of their body weight, while those on the placebo lost only 2%. Although further research is needed to fully uncover the mechanisms behind the treatment, it may also directly target the processes driving the disease.
“It’s not yet established, but part of the efficacy of GLP-1-like drugs might be due to their effects on immune cells and reduction of inflammation,” notes Newsom.
Antibiotics commonly used to absorb pneumonia remove Lyme disease mice at doses 100 times lower than standard antibiotic therapy. This small dose was combined with the targeted effect of the drug on infection, meaning that the animal’s gut microbiota was largely unaffected.
Lyme disease is caused by bacteria in the genus Borelia It spreads mostly among birds and small rodents, but people can get infected via the bites of mites that have given the blood of such animals. Infections generally lead to flu-like symptoms and a “bull” rash. Without treatment, it can cause serious long-term complications such as fatigue and pain.
Standard treatment involves taking the antibiotic doxycycline twice daily at high doses for up to three weeks. This will stop the production of the proteins needed for bacteria to survive, but will not selectively target them Borelia seed. “It will cause chaos normally [gut] It says microbiome. Brandon Footlas At Northwestern University, Illinois.
Looking for a more selective alternative, Jutras and his colleagues first tested how effective it is to have more than 450 antibiotics all approved by the US Food and Drug Administration. Borrelia burgdorferi – The most common type of lab dishes that causes Lyme disease.
They then evaluated how best-performing drugs affected the growth of harmless or beneficial bacteria commonly found in people and mouse visceral organs, such as certain strains. E. coli. This revealed that piperacillin is associated with penicillin, commonly used in the treatment of pneumonia and is the most selective target. B. burgdorferi.
Next, the researchers injected 46 mice. B. burgdorferi. Three weeks later, they treated the animals with various doses of either doxycycline or piperacillin for a week. The researchers found that mice received either high doses of doxycycline or 100 times lower doses of piperacillin, with no signs of infection.
They also analyzed stools from mice before and after antibiotic treatment and found that low doses of piperacillin had little effect on bacterial levels. B. burgdorferi In the gut, high doses of doxycycline significantly altered the gut microbiota.
This is probably due to the low amount of antibiotics, which has less impact on intestinal microbial diversity and is the target action of piperacillin. “We found that using piperacillin is targeting certain proteins. B. burgdorferiit is very efficient to kill this Lyme disease agent at low concentrations, not other bacteria, to survive,” says Jutras.
But mice can respond differently to antibiotics than people, John Ocotte at Johns Hopkins University in Maryland. For example, they often break down the drug faster, which can change its effectiveness. The Jutras team hopes to test piperacillin in human Lyme disease tests in the coming years.
According to Borghammer’s “Aha” moment, it came almost 20 years ago. Neuroscientists were reading papers from researchers investigating REM sleep behavior disorders (RBD). This is a condition in which people develop dreams, often discovered in people who develop Parkinson’s disease, and may be a form of early neurological symptoms.
However, rather than starting from the brain, the team looked for the loss of nerve cells in the heart instead. Parkinson’s disease has historically been linked to depletion of neurons in the brain, but it also affects cardiac neurons that manage autonomic nervous functions such as heart rate and blood pressure. And say Borgamer“In all these patients, the heart is invisible. It’s gone.”
Of course, it’s not literal. However, in these people, neurons that produce the neurotransmitter norepinephrine, which helps control heart rate, were depleted to the point that the heart did not appear on scans using radioactive tracers. This type of neuronal loss is linked to Parkinson’s disease, but no one was diagnosed with the disease at the time, and brain scans appeared to be normal.
What struck Borghammer was that Parkinson’s disease appears to have not followed the same trajectory in all affected people. Although RBD strongly predicts Parkinsonson’s predictions No one has Parkinson’s experience. RBD.
The sun smashed through the sandstone arches of window rocks in northeastern Arizona, and Health Secretary Robert F. Kennedy Jr. of Blue Jeans finally became his element: Hiking.
It was his final day of his multi-state Make American Healthy Tour. It is designed to highlight various aspects of Kennedy’s plan to combat chronic illness, including healthy school lunches and clinics, which take a holistic approach to patient care.
Currently, the Health Secretary is on a walk with the Navajo president, representatives of the National Council and representative director of Indian Health Services, discussing the challenges of providing quality health care to tribal groups. Here, weaving in the desert brush, Mr. Kennedy seemed to be striking his journey.
Kennedy had left Washington on questions about the handling of measles outbreaks in western Texas and the firing of thousands of Department of Health and Human Services employees. On his way out west, he had to stop by Texas on Sunday to attend the funeral of an 8-year-old who had not been vaccinated.
And at the start of the tour the following day, Kennedy looked stoic as he was led by Salt Lake City Health Center, focusing on nutritious diets. He declined a bag of fresh groceries, citing upcoming flights. In “Training Kitchen,” he dropped ice cubes, dribbled mango lassi, and stood faceless as the medical students reached to activate the secretary’s food processor without a lid. (The administrator stopped her just in time.)
“That would have been a bad thing,” the student said. I glanced at the secretary’s white shirt and pressed my suit. Finally, Kennedy broke a smile.
By Tuesday, Kennedy had loosened, wearing a stegosaurus tie at a health center near Phoenix and shaking hands with a Navajo toddler. The Health Secretary thrusts his head into the food distribution centre’s refrigerator, looks up the food label and nods “very impressive.”
There was one minor fake PA at a tribal conference of 1,300 people who tried to show off their knowledge of dress for Wampanoag, who lives in Cape Cod and Martha’s Vineyards in Massachusetts. (“My home tribe,” he said.) When he spoke from the glittering casino stage, he pointed out the tribe’s chairman’s traditional Shellbead earrings and necklaces, and announced, “If you want to know what Wampum originally looked like, she’s a museum piece!” (She was breathless.)
At a press conference on the school lunch assembly at the Arizona State Capitol, Kennedy was adjacent to dozens of school children. There was a loud applause, “I’m off to Bobby!” a chant from behind. By then he was shining.
On the hiking trail Wednesday morning, Kennedy got a glimpse of the persona he once exhibited on the presidential trail. From heroin addiction By throwing yourself into a new extreme.
He first scrambled towards the top of the window rock formation, a balanced silhouette of 1,000 feet of the valley floor.
When it comes to his own battle with chronic illness, Kennedy relies on natural diet, intermittent fasting, and morning routines such as 12-step meetings, gym time, and meditation. However, since arriving in Washington, he had to give up his favorite daily ritual. It’s a 3-mile hike with your dog.
On the trek, authorities discussed initiatives like the Navajo long-standing 2% tax on junk food, which was adopted as part of a law passed in 2014. They also spoke about the Navajo Agricultural Industry, a tribal program that sells corn, beans and other products under the “Navajo Pride” brand to support the community.
To close the tour in the southwest, Kennedy visited the Hózhó Academy in Gallup, New Mexico, a K-12 school that hosts family-friendly gardening and cooking events and uses the curriculum to help students plan their own health goals.
Epidemiologists say there are factors that promote the rate of promotion of chronic disease, such as genetics, altered gut microbiota, and the fact that Americans generally live longer and therefore face new conditions with age.
Kennedy says there is a tendency to deemphasize these factors, and these experts say they have instead focused on childhood vaccine schedules, psychiatric medications and other variables. But here on the tour, Kennedy maintained most of his personal health attention as an important way to deal with the crisis.
The enthusiasm of the secretary taking on a large food company seems to match more with the traditional political left than the right. As he called it, the fight against artificial food dyes called “poison” is an echo of existing California law, and his school visits are reminiscent of Michelle Obama’s Let’s Move! A campaign to take on obesity in children.
For some, Kennedy’s advocacy of healthy food laws comes at a paradoxical moment. This is because last week the Food and Drug Administration’s extensive layoffs included lab scientists who tested contaminant foods. The administration also eliminated major food safety commissions and cut funding for state-based food inspectors.
And Kennedy promoted chronic disease prevention, which eliminated important efforts like the 29-year-old research initiative, the Diabetes Prevention Program. On his descent from the hike, a representative from the Navajo Council of States, struggling to get his diabetes medication, intercepted the secretary, unzipped his jacket and revealed the t-shirt with handwritten phrases. (IHS stands for Federal India Health Services.)
“A subtle message,” she said.
Kennedy promised her that he would talk to his team and see what he could do. She tied her arms to Kennedy, who was worried about maintaining Kennedy’s balance, and put it all the way down.
In the 1960s and 1970s, Kilmer S. McCurry, a pathologist at Harvard Medical School, was controversially expelled into the basement. He claimed that the amino acid homocysteine had been overlooked as a potential risk factor for heart disease.
His daughter, Martha McCurry, later revealed that he passed away due to metastatic prostate cancer. His death was not widely reported at the time.
Dr. McCurry’s theory, which is still debated, suggested that inadequate vitamin intake could lead to high homocysteine levels in the blood, causing plaque buildup and artery stiffening. This challenged the prevailing cholesterol-centric view supported by the pharmaceutical industry.
Although Dr. McCurry acknowledged the importance of cholesterol, he believed homocysteine should not be ignored. However, his superiors at Harvard disagreed, leading to his lab being moved underground and eventually being told to leave.
In a 1995 interview, Dr. McCurry described his experience as “very traumatic.” He felt isolated and misunderstood by his peers.
At a medical conference in Boston, Dr. McCurry learned about Homocystinuria, a genetic disorder linked to high homocysteine levels. This discovery sparked his interest in the role of homocysteine in disease.
One case involving a young girl with homocystinuria who had a family history of the disease stood out to Dr. McCurry. This prompted him to further investigate the connection between homocysteine and artery stiffness.
“How did an 8-year-old die in the way an elderly man?” Dr. McCurry wrote in The Heart Revolution, recalling the incident that led to his controversial research. credit…HarperCollins
After studying tissue samples, Dr. McCurry found evidence that homocysteine could lead to artery stiffening without cholesterol or fat buildup. This discovery further fueled his research into homocysteine’s role in heart disease.
The rejection of Dr. McCurry’s theory in the 1960s and 1970s took a toll on his career. He struggled to find employment for years after leaving Harvard.
Despite facing resistance, Dr. McCurry continued his research on homocysteine and its impact on heart health. His persistence ultimately paid off, as studies in the 1990s confirmed his earlier findings.
Dr. McCurry’s work shed light on the importance of homocysteine as a marker for cardiovascular disease risk. His perseverance and dedication to his research have since been acknowledged by the medical community.
Dr. McCurry’s early research laid the foundation for later studies linking homocysteine levels to heart disease risk. Subsequent investigations have supported his initial claims, validating his work and legacy in the field of cardiology.
Despite initial skepticism, Dr. McCurry’s contributions to the understanding of homocysteine have been recognized by the medical community. His insights have paved the way for further research into the role of this amino acid in cardiovascular health.
Dr. McCurry’s groundbreaking work continues to inspire researchers and clinicians to explore the complex relationship between homocysteine and heart disease. His legacy lives on in the ongoing pursuit of innovative approaches to cardiovascular care.
Quantum physics is confused. Luckily, scientists have been exploring it for years, and finally we are beginning to understand it all. Quantum Mechanics guide now easier. A Whistlestop tour to understand the basic theory that governs very small things.
Near-death experience
They left their bodies, witnessed a bright light, and returned forever. But will the survivors of near-death experiences (NDEs) get a glimpse of something great beyond that? Here’s what NDES can tell us about the mystery of our final moments:
Losing the world under the sea
Discover the lost landscape off the coast of Australia, engulfed in the ocean that could have lived over half a million years ago.
Mystical signals from deep space
Fast Radio Burst: Are these mystical signals from deep spaces becoming even more strangers?
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There’s a bit of hope: Having hope is a way to do better for your mental health than mindfulness.
New pieces of obesity puzzle: A better understanding of the human hypothalamus pathways has great medical potential and could lead to new treatments of obesity.
Q&A: Your question answered! This month: Does your name affect your physical appearance? Does something poop gold? How old is Jupiter’s Great Red Spot? Why is it so difficult to switch tasks? What’s the craziest thing ever stolen? And more!
Parkinson’s disease is rapidly becoming one of the most prevalent neurodegenerative conditions globally, impacting over 10 million individuals worldwide. It ranks as the second most common neurodegenerative ailment following Alzheimer’s disease. As of now, there is no known cure. However, recent advancements have raised hopes for the development of new treatments in the near future.
The disease is closely associated with a protein known as Pink1, which carries a mutation in the Park6 gene responsible for encoding this protein.
Malfunctions in Pink1’s functioning are directly linked to Parkinson’s disease, especially in individuals with early onset, affecting 1.2% of Parkinson’s patients in the UK.
Recent scientific progress has shed light on the interaction between Pink1 and mitochondria. Mitochondria, known as the powerhouse of cells, produce energy within the cells of all organisms.
From left, Professor David Commander, Dr. Nicholas Kirk, Dr. Sylvie Karegari and Dr. Alisa Grukova stand before the discovery of Pink 1. – Wehe
The link between Pink1 and Parkinson’s disease has long been recognized, but its potential as a cure for Parkinson’s disease has only recently been explored.
When mitochondria are damaged, Pink1 signals the need for their removal. However, in Parkinson’s patients, mitochondrial defects accumulate unnoticed, releasing toxins that eventually lead to cell death.
Currently, researchers at the Parkinson’s Center for Research in Walter and Eliza Hall (WEHI) in Australia have elucidated the structure and activation process of Pink1. Their findings on how Pink1 interacts with dysfunctional mitochondria are published in Science today.
“This is a significant milestone in Parkinson’s disease research,” stated corresponding author Professor David Commander, head of WEHI’s ubiquitin signaling division. “Understanding Pink1’s binding to mitochondria is truly groundbreaking.”
Lead author and Senior Researcher at WEHI, Sylvie Callegari, explained that Pink1 functions in four distinct steps, with the first two being newly discovered in this study.
Furthermore, Pink1’s role in detecting mitochondrial damage and initiating the process of mitophagy, the recycling of damaged mitochondria, is crucial for addressing Parkinson’s disease.
Parkinson’s disease is associated with physical tremors, as well as other symptoms like language and vision impairments – Credit: Witthaya Prasongsin
In conclusion, understanding the Pink1-mitochondrial relationship is crucial for developing therapies for Parkinson’s disease, a condition characterized by the decline of brain cells.
Given the increasing prevalence of Parkinson’s disease over the past 25 years, the need for effective treatments is more urgent than ever. The researchers behind this study aim to accelerate drug development and halt the progression of Parkinson’s disease.
Neuroscientist David Levitin explores how music can help us heal in new book
Natalie Foss
Most of us already know that music can have a profound effect on the mind and body. Think about the feeling of empowerment when you put on your headphones and go for a run, the nostalgia of hearing your favorite songs from your childhood, or the joy of singing in the car. Music moves us both literally and figuratively. It not only makes us dance, laugh and relax, but it also makes us happy when we are sad and sad when we are happy.
But what if there is more to it than that? What if music actually has the power to heal us? In his new book I heard there’s a secret code: music as medicine, neuroscientist Daniel Levitin explains why he believes it’s possible.
The idea that music is medicine is not new. There is evidence that shamans and healers from cultures around the world have used music, especially drumming, to heal people for thousands of years.
However, it is only in recent decades that science has provided a rationale for music as a healing mechanism, demonstrating that music has a direct and measurable effect on our nervous systems.
Advances in neuroimaging technology, combined with more rigorous experiments based on music theory, cognitive psychology, and physiology, are showing that music could help treat everything from Parkinson’s disease to Alzheimer’s disease to depression. Levitin spoke with new scientist to learn about these health benefits and how music can add to your medical toolkit.
Linda Rodriguez McRobbie: Intuitively it seems like…
in new research Published in a magazine frontiers of public healthScientists surveyed 69,705 participants (47.2% women) aged 45 to 83 from the Swedish Mammography Cohort and the Swedish Men's Cohort to assess their intake of added sugars and a variety of sugary foods and beverages. We investigated the association between this and the risk of seven cardiovascular diseases. Researchers have found that eating too much added sugar increases the risk of stroke and aneurysm, but eating small snacks lowers the risk of cardiovascular disease. On the other hand, drinking sugary drinks increases your risk of stroke, heart failure, and atrial fibrillation.
Although additional sugar intake was positively associated with ischemic stroke and abdominal aortic aneurysm, the lowest intake categories had the highest risk for most outcomes. Positive linear associations were found between topping intake and abdominal aortic aneurysm, and between sweetened beverage intake and ischemic stroke, heart failure, atrial fibrillation, and abdominal aortic aneurysm. There is no relationship between snack intake (pastries, ice cream, chocolate, sweets) and all outcomes, and between topping intake (sugar, honey, jam, marmalade) and heart failure and aortic stenosis. , a negative linear correlation was found. Image credit: Ernesto Rodriguez.
Cardiovascular disease comprises a variety of diseases of the heart and blood vessels and is currently the leading cause of death and disease burden in Europe, mainly due to stroke and ischemic heart disease.
Although diet is one of the main modifiable risk factors for many CVDs, evidence regarding added sugar intake and CVD risk is lacking and inconclusive.
Additionally, most studies have primarily focused on sugar-sweetened beverage consumption rather than total added sugar intake, even though sugar-sweetened beverages account for 14% of added sugar intake in Sweden and only 25% in the United States. I'm guessing.
“The most surprising finding of our study was the differential relationship between different sources of added sugar and CVD risk,” said Suzanne Junge, a PhD candidate at Lund University. That's what I mean.''
“This striking contrast highlights the importance of considering not only the amount of sugar consumed, but also its source and context.”
To understand how sugar intake affects cardiovascular disease risk and whether those risks change with intake of different types of sugar, Janzi et al. Data were collected from two major cohort studies: a cohort of men and a cohort of Swedish men.
These studies administered dietary questionnaires in 1997 and 2009, allowing scientists to monitor participants' diets over time.
Once exclusions were made to ensure the two cohorts shared the same inclusion criteria and remove independent risk factors for CVD, researchers were left with a sample of 69,705 participants .
They identified three classes of sugar intake: toppings such as honey, treats such as pastries, and sugary drinks such as soda, and two different types of stroke, heart attack, heart failure, aortic aneurysm, atrial fibrillation, and aortic stenosis. investigated seven CVDs. .
Participants were monitored until death, diagnosis of CVD, or end of follow-up in 2019.
During this period, 25,739 participants were diagnosed with CVD.
The scientists then used this data to analyze how different types of sugar intake affected the risk of various CVDs.
They found that consuming sugary drinks is worse for your health than any other form of sugar. Drinking more sugary drinks significantly increases your risk of ischemic stroke, heart failure, atrial fibrillation, and abdominal aortic aneurysm.
“The liquid sugar found in sweetened beverages is typically less satiating than solid foods, which can lead to less satiety and overconsumption,” says Junge.
“Context is also important. Snacks are often enjoyed during social gatherings or special occasions, while sugary drinks may be consumed more regularly.”
Different types of CVD are affected differently by increased sugar intake. This is likely because added sugar intake has a different impact on participants' individual risk profiles.
Increased carbohydrate intake generally increased the risk of ischemic stroke and abdominal aortic aneurysm, and also increased the risk of heart failure in participants with a normal BMI.
However, the category with the lowest snack intake had the highest risk of negative health outcomes. Occasional snacking was associated with better outcomes than no snacking at all.
“This may reflect underlying dietary habits. People with very low sugar intake may have very restrictive diets, or may have low sugar intake due to pre-existing health conditions. may be limiting,” Junge said.
“Although our observational study cannot prove causation, these results suggest that extremely low carbohydrate intake may not be necessary or beneficial for cardiovascular health.”
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Suzanne Junge others. 2024. Added association between sugar intake and incidence of seven different cardiovascular diseases in 69,705 Swedish men and women. frontiers of public health 12;doi: 10.3389/fpubh.2024.1452085
Don’t panic! Disease X doesn’t exist yet, but it might someday. Disease Coined in 2017, the term can be used to mean a newly discovered pathogen or a known pathogen with newly acquired pandemic potential. According to the latter definition, covid-19 was the first disease X. However, in the future another disease may appear.
Why are people talking about it now?
The World Health Organization is warning world leaders about the risk of future pandemics at the World Economic Forum’s annual meeting. “Some people say this could cause panic,” says WHO director-general Tedros Adhanom Ghebreyesus. “No. It’s happened so many times in our history that it’s better to anticipate what might happen and be prepared for it.”
What will be the next disease, X?
We don’t know – that’s why it’s called Disease X. Coronaviruses, a large group of viruses, have long been seen as prime candidates for causing new pandemics, even before the COVID-19 outbreak. That’s because the new coronavirus was not the first dangerous pathogen in this group. In 2002, another coronavirus began to spread in China. It caused a type of pneumonia called SARS, which killed about one in 10 people who contracted it, before being stopped by strict infection control measures. Another more deadly coronavirus, called MERS, occasionally occurs and causes pneumonia that kills one in three people infected. However, recent research suggests that it will be more difficult for SARS and MERS to cause new pandemics. This is because almost everyone in the world now has antibodies against the virus that causes Covid-19, and these have partial resistance to most other pathogens in the coronavirus family. This is because it seems to provide protection.
Are there any other candidates with pandemic potential?
Many diseases, some well-known and some less well-known, can pose a global threat. Influenza strains have caused several global pandemics in the past, including the 1918 Spanish flu, one of the deadliest diseases in history. A highly virulent avian influenza virus is currently sweeping the world, and birds can sometimes infect mammals. causing mass deaths. Just this week, he was named as the culprit behind the deaths of 17,000 baby elephant seals in Argentina last October. There are other sources of infection, including Ebola, which causes severe bleeding, and Zika, a virus transmitted by mosquitoes that can cause babies to have smaller heads if infected during pregnancy. WHO updated its report List of pathogens with the highest pandemic potential In 2022.
What can be done to stop disease X?
There’s some good news. The COVID-19 pandemic may have made it easier to stop future Disease X outbreaks. COVID-19 has spurred the development of new vaccine designs, including vaccines that can be quickly reused to target new pathogens. For example, this has led to the emergence of mRNA-based vaccines. The formula contains a short piece of genetic material that causes the body’s immune cells to produce the coronavirus “spike” protein, but it can be updated to allow the cells to mass-produce a different protein by simply rewriting the mRNA sequence. There is a possibility that it can be done.
Is there anything else I can do to fight disease X?
Mr Tedros said countries needed better early warning systems for emerging diseases and health services needed to be more resilient to unexpected spikes in demand. “When hospitals exceed capacity, [with covid]we lost a lot of people because we couldn’t manage them. There wasn’t enough space and there wasn’t enough oxygen. ” Tedros said health services must be able to scale up response capacity on demand to avoid the same thing happening when Disease X occurs. Fortunately, they can make such preparations without knowing exactly what disease X is. “Disease X is a placeholder,” he says. “You can prepare for any illness.”
A mysterious illness with flu-like symptoms has claimed the lives of dozens of people in the Democratic Republic of Congo, as reported by the country’s health authorities.
As of Tuesday, the unknown disease has resulted in the death of 79 people and the sickness of 376 individuals, according to the country’s Ministry of Public Health, Hygiene and Social Security.
In a statement regarding X, the ministry stated that the origin of the disease is “still unknown” and was first identified in Kwango province in southwestern Congo.
Symptoms reported include fever, headache, stuffy nose, cough, difficulty breathing, and anemia.
According to Reuters and Associated Press, local authorities have warned that the death toll could potentially rise to 143.
The Ministry of Health emphasized that the remains of those who have died with similar symptoms should not be handled without the involvement of authorized health authorities. They urged the public to report any suspicious illnesses or unusual deaths, avoid large gatherings, and follow basic hygiene practices like washing hands with soap and water.
Emergency public health officials are being deployed to the affected area, as confirmed by the ministry.
The World Health Organization, in response to the reports of the unidentified illness, stated to NBC News that they are collaborating with local authorities and have dispatched a team to collect samples for laboratory testing.
The U.S. Centers for Disease Control and Prevention, with offices in Congo, is aware of the situation and is providing technical support to a rapid response team sent by the local emergency operations center.
Alzheimer’s disease is, understandably, one of the most feared diseases of old age. It robs people of their memories, places a tremendous strain on caregivers, and imposes a huge economic burden on both individuals and society. Tens of millions of people have already been diagnosed with Alzheimer’s, and if predictions are correct, that number will more than double by 2050.
Until recently, it seemed there was no hope of averting this catastrophe, but rapid advances in medical science have made it realistic prospects that Alzheimer’s may be treatable and eventually eradicated (see “A new kind of vaccine could lead to Alzheimer’s eradication”).
The first of a new class of drugs is already creating buzz, but not necessarily for the right reasons. Last week, the UK’s Medicines and Healthcare products Regulatory Agency approved the drug, called lecanemab. But NICE, the body that advises on whether new treatments are cost-effective, has made a provisional decision that taxpayers will not fund the drug in England. No decision has yet been made in the rest of the UK.
This is obviously a tough pill to swallow for Alzheimer’s patients and their families. But in the grand scheme of things, this is good news. Lecanemab is not a particularly effective drug. Its effects are modest, it has serious side effects, and it is expensive. But it does show that the causes of Alzheimer’s are now understood and treatable. This is further reinforced by the fact that the drug is also approved in the United States and Japan, but the European Medicines Agency has refused to approve it.
So the way is almost paved for the next wave of drugs to target the causes of Alzheimer’s, which could be ready around 2030. These are vaccines, not in the traditional sense of conferring immunity against an infection, but they work in essentially the same way, by stimulating an immune response against the misfolded proteins that cause the symptoms of Alzheimer’s. The first vaccines will be therapeutic, slowing or stopping the progression of Alzheimer’s, but the next generation will be preventative, preventing the onset of Alzheimer’s. Eventually, the only memory that will fade will be Alzheimer’s itself.
A recent study suggests that living in a neighborhood filled with trees can have similar heart benefits to regular exercise. Researchers at the University of Louisville conducted a clinical trial involving hundreds of people living in six low- to moderate-income neighborhoods in South Louisville, Kentucky. They found that planting thousands of mature trees near people’s homes led to lower levels of blood markers associated with heart disease, diabetes, and some cancers.
The Green Heart Louisville Project, part of the HEAL Research, revealed that areas with more trees and shrubs had improved health outcomes compared to areas with fewer trees. This study aimed to reduce the incidence of heart disease in the community under the leadership of Professor Aruni Bhatnagar.
Unlike previous observational research, the HEAL study had a control group and an intervention group, providing clearer insights into the effects of nature. Participants aged 25 to 75 living in South Louisville were recruited for the study, with samples collected before and after the tree-planting intervention.
The results showed a 13% decrease in a blood marker associated with heart disease in individuals living in areas with more trees. This reduction was comparable to the benefits seen from starting a regular exercise routine.
Overall, the study demonstrated a strong link between trees and improved physical health by providing shade, cooling, and noise reduction. Beyond physical health, trees also offer mental health benefits and create spaces for relaxation, exercise, and socialization.
How trees improve your physical health
Trees play a crucial role in mitigating urban heat and air pollution, which can worsen existing health conditions. The project in South Louisville focused on areas with poor air quality to study the impact of tree planting on pollution levels.
As the project continues, researchers plan to expand tree planting to other areas and explore additional benefits such as encouraging outdoor activities and improving overall well-being. The findings highlight the importance of equitable access to green spaces in cities and the essential role of nature in human health.
In conclusion, nature is not just a luxury but a necessity for human well-being, and efforts should be made to ensure everyone has access to green spaces for a healthier future.
Doctors are calling for a ban on artificial stone, a popular material used for kitchen worktops, following the confirmation of eight cases of artificial stone silicosis in the UK for the first time.
Also known as engineered or reconstituted stone, artificial stone has gained popularity for its aesthetics and durability over the last two decades. However, a new report published in the British Journal of Construction highlights the serious health risks posed by its high silica content, which exceeds 90% compared to 3% in marble and 30% in granite.
“Silicosis is a progressive lung disease caused by inhaling crystalline silica dust,” said Dr. Patrick Howlett, a spokesperson for BBC Science Focus. “The risk of developing silicosis is significantly higher for workers in the artificial stone industry compared to those with chronic respiratory conditions.”
“Various industries expose individuals to silicosis, including mining, pottery, cement work, and now artificial stone fabrication. Prolonged exposure to low levels of silica dust can lead to the development of silicosis over time,” added Dr. Howlett.
All eight affected individuals were male, with an average age of 34, and most worked for small businesses with fewer than 10 employees. Poor safety practices, such as inadequate respiratory protection and ventilation systems, were reported by workers during cutting and grinding operations.
The report’s authors emphasized the need for national guidelines and better enforcement to protect workers from artificial stone silicosis. They highlighted the urgent need for early detection of cases and preventative measures to avoid a potential epidemic.
Since 2010, cases of artificial stone silicosis have been reported worldwide, but the UK confirmed its first cases in mid-2023. California has identified nearly 100 cases of silicosis among countertop workers, prompting the adoption of new regulations to safeguard workers.
Australia has already banned the use of artificial stone as of July 2024, aiming to eliminate the health risks associated with its production and installation.
In related editorials, Dr. Christopher Barber and researchers from Sheffield Teaching Hospitals NHS Foundation Trust drew parallels between artificial stone silicosis and historical occupational health crises, urging stricter regulations and enforcement to protect workers.
Experts are currently reviewing exposure limits for crystalline silica dust in the UK, with a focus on mitigating the risks associated with artificial stone worktops. Silicosis remains a significant concern for clinicians and researchers in the occupational health field.
About our experts
Patrick Howlett: An MRC Clinical Research Fellow at the National Heart and Lung Institute, Imperial College London, focusing on silicosis and tuberculosis among small-scale miners in Tanzania.
Christopher Barber: A leading expert in occupational and environmental lung disease, serving as a medical advisor to the UK Health and Safety Executive and conducting extensive research in the field.
Green and gold bell frogs in an artificial hotspot shelter
Anthony Waddle
One of Australia’s most endangered amphibians can fight off a deadly fungal infection with the help of a naturally heated shelter that researchers are calling a “frog sauna.”
The disease, chytridiomycosis, has wiped out about 100 species of frogs, toads and salamanders worldwide.
Green and gold bell frog (Litoria aureaThe fungus was once widespread along the south-eastern coast of Australia, but its range has shrunk by 90 percent, and although other factors such as habitat loss are also at play, chytrid is thought to be the greatest threat to the endangered species.
It has long been known that warm temperatures suppress fungal infections, and many frog species, including the Japanese bush frog, are susceptible to the disease in winter when it’s hard for them to stay warm, especially when it’s hard to find a warm place.
To learn more, Anthony Waddle The researcher, from Macquarie University in Sydney, and his colleagues studied two groups of captive frogs that were intentionally infected with chytridiomycosis over the winter.
The first group was provided with bricks with holes in them in an unshaded greenhouse shelter where temperatures rose to nearly 40°C (104°F), while the second group was provided with bricks in a shaded greenhouse shelter where temperatures rose to 35°C (95°F).
Frogs that were given warmer shelter had 100 times fewer chytrid spores on their skin than other groups.
Although chytrid has difficulty growing above 28°C (82°F), warmer temperatures appear to activate the frogs’ immune systems, Waddle said.
“Using shelter to survive is like a vaccination for the frogs,” Waddle says, “and we’ve shown that firefly frogs can develop resistance after heat has cleared their infection, potentially making them 22 times more likely to survive future infections in cold environments.”
Although the researchers have only tested the shelter on one species at this stage, they believe the technology could be used with other animals threatened by chytrid fungus, as long as they seek out natural warmth when it’s cold. Waddle says there are at least six Australian animal species that could benefit from the technology.
Importantly, these thermal shelters are easy and inexpensive to set up: “All you need is a small vegetable greenhouse from the hardware store and a few bricks, and it will only cost about $60-70. [Australian] “It will cost a few hundred dollars to build,” Waddle said, “and I can envision people putting them in their backyards to help the frogs through the winter.”
Research on families with early-onset Alzheimer’s disease has revealed a genetic abnormality that can delay early symptoms by five years. This finding paves the way for a new approach to combating the disease by potentially leveraging the protective effects of this gene mutation. A very rare genetic mutation offers some hope in the fight against Alzheimer’s.
Scientists first noticed this genetic protection in a Colombian family afflicted with a hereditary form of Alzheimer’s disease. They identified a woman, Aliria Piedrahita de Villegas, who should have developed symptoms in her 40s but remained symptom-free well into her 70s. She carried an unusual genetic combination, including two copies of the APOE3 gene with a mutation known as Christchurch, which seemed to provide her with protection against Alzheimer’s.
Further research identified 27 individuals with one copy of the Christchurch variant, showing that having one copy delayed the onset of cognitive impairment by an average of five years compared to their relatives. The study, published in the New England Journal of Medicine and involving researchers from various institutions, provided hope that correcting this gene could potentially slow the progression of Alzheimer’s.
Notably, Alzheimer’s typically affects older individuals, with risk increasing with age. The APOE gene has long been associated with the disease, with certain variants like APOE4 increasing risk. However, the Christchurch variant appears to play a protective role, potentially preventing the accumulation of the proteins amyloid and tau that are linked to Alzheimer’s.
The study included brain scans and autopsy results from individuals with the Christchurch gene, shedding light on its potential impact on Alzheimer’s progression. While there is still much to learn about this rare mutation and its effects, there is optimism that it could offer insights into treating Alzheimer’s and potentially delaying its onset.
Ellagic acid is a polyphenolic, non-flavonoid compound found naturally in a variety of fruits, including pomegranates, raspberries, strawberries, and grapes, as well as nuts, including pistachios, pecans, walnuts, and acorns.
Senavirasna othersResearchers are investigating the effects of ellagic acid, an antioxidant found in pomegranates, raspberries, strawberries, grapes and nuts, in preventing and potentially reversing the damage caused by fatty liver disease. Image courtesy of Engin Akyurt.
Obesity is epidemic in many parts of the world and contributes to increasing rates of non-alcoholic fatty liver disease (NAFLD).
This rapidly expanding epidemic is the most common chronic liver disease worldwide.
The prevalence of NAFLD increased from 25.24% in 2015 to 29.38% in 2021.
NAFLD represents a range of pathologies from simple fatty liver (nonalcoholic fatty liver, NAFL) to nonalcoholic steatohepatitis (NASH), which can progress to more severe conditions including fibrosis.
Currently, no cure exists for the long-term management of NAFLD/NASH, but dietary interventions containing several polyphenolic compounds have been investigated for the treatment of NASH. Ellagic acid is one such compound.
“Ellagic acid, found in a variety of foods including raspberries, pomegranates, blackberries and pecans, is widely known for its antioxidant properties but has also demonstrated anti-inflammatory, anti-fibrotic and anti-cancer properties,” said researcher Lois Balmer and doctoral student Tarani Senaviratna, both from Edith Cowan University.
“Ellagic acid stands out as a remarkable polyphenolic compound with a wide range of pharmacological properties that may be promising for the treatment of various chronic diseases, including NAFLD.”
“Edible plants containing ellagic acid and its derivatives are recognized as valuable functional foods that promote human health due to their pleiotropic biological effects.”
“Furthermore, evidence suggests that ellagic acid may exert synergistic therapeutic effects when combined with other antioxidant dietary supplements, making it a potential candidate for combination therapy.”
The authors were involved in a previous pilot study investigating the effects of several polyphenolic compounds on NAFLD, with ellagic acid showing the most promise in reducing inflammation.
“Ellagic acid exerts its hepatoprotective properties mainly through scavenging free radicals, modulating cytokine production, and regulating lipid metabolism,” the researchers said.
“Ellagic acid, a potent antioxidant, combats reactive oxygen species (ROS) and activates the NrF2 pathway to reduce oxidative stress and protect the liver.”
“Surprisingly, ellagic acid also inhibits the Nf-kB and MAPK pathways, reducing inflammation during NAFLD/NASH.”
“Evidence also shows that ellagic acid can lower both triglyceride and cholesterol levels and combat de novo lipogenesis, a significant risk factor in the progression of NASH.”
“Test-tube findings suggest that ellagic acid has the ability to reduce fibrosis.”
“Urolithins, the main microbial metabolites of ellagic acid, have been shown to improve the gut microbiota in several mouse models of obesity.”
“Specifically, Urolithin A has been shown to lower LDL and increase HDL levels and is also involved in improving lipid metabolism through gene regulation, while Urolithin C activates the hepatic AMPK pathway, countering the pathophysiology of NAFLD.”
“While the health benefits of ellagic acid and urolithins in NAFLD/NASH are being debated, their biological effects on the liver are still poorly understood.”
“Given that lipid metabolism, oxidative stress, inflammation, and insulin resistance play a role in the development of NASH, the results of this review suggest that ellagic acid may be a potential dietary intervention for NASH, potentially suppressing and even reversing the pathological symptoms of NAFLD/NASH.”
Tarani Senavilasna others2024. Elucidation of the therapeutic effects of ellagic acid on nonalcoholic fatty liver disease and nonalcoholic steatohepatitis. Antioxidants 13(4):485; doi:10.3390/antiox13040485
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