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
Aggregates of protein α-synuclein (brown) and antibody (green)
Biolution GMBH/Science Photo Library
Drugs that target protein accumulations associated with Parkinson's disease may slow the progression of motor symptoms in patients with advanced Parkinson's disease. This shows potential as a disease-modifying treatment for Parkinson's disease, but it is unclear whether the drug actually removes the protein from the brain.
Accumulation of a misfolded protein called alpha-synuclein in the brain has long been thought to be the underlying cause of Parkinson's disease. This results in the loss of neurons that produce the neurotransmitter dopamine, which is involved in motor control.
Some existing treatments aim to alleviate these symptoms by improving dopamine levels in the brain, but their long-term effects are limited. To date, there are no approved disease-modifying treatments to stop or slow the progression of Parkinson's disease.
In an effort to counter this, Gennaro Pagano Swiss pharmaceutical company Roche and colleagues recruited 316 people who appeared to have early stages of Parkinson's disease. Of these people, 105 received an intravenous infusion of a placebo, and 211 received a low or high dose of Roche's drug plasinezumab every four weeks for a year.
Placinezumab is an antibody designed to bind to aggregates of misfolded alpha-synuclein within dopaminergic neurons. “It is hypothesized that placinezumab may reduce neurotoxicity, prevent cell-to-cell movement of pathological alpha-synuclein aggregates, and slow disease progression,” Pagano says.
Trial results initially suggested the antibody had no significant effect, but the team later realized it may have an effect in trial participants with more severe forms of Parkinson's disease. I did.
These people suffered from rapid eye movement sleep behavior disorder, which causes intense, often violent dreams that are common in Parkinson's disease. He was taking a drug called an MAO-B inhibitor to manage his symptoms. Or, he has been rated by an expert at 2 out of 5 on a symptom scale, with higher numbers indicating greater severity.
Additional analyzes showed that both low and high doses of the drug had greater effects than seen in the first study, especially among critically ill participants. The rate at which participants' motor symptoms worsened over a one-year period was significantly reduced compared to those taking a placebo.
For example, based on the Parkinson's Disease Rating Scale for Motor Symptoms, patients who took an MAO-B inhibitor and then received a placebo infusion had a score of 6.82 at the end of the year, compared to Patients who took the drug had a score of 4.15.
“These results suggest that potential treatment benefits may be more likely to be achieved in populations that experience greater deterioration over time and more rapid progression,” Pagano says. This is because patients with Parkinson's disease, which progresses more rapidly, have higher amounts of misfolded alpha-synuclein in their brains, so they may benefit more from drugs that can remove this protein. There is a possibility.
However, Professor Pagano said researchers lacked a biomarker that could monitor how participants' levels of misfolded alpha-synuclein changed, so it was unclear what was happening in the participants' brains. He said it was not possible to make an accurate assessment.
Vinata Vedam Mai Researchers at the University of Florida Health say a limitation of the study is that it did not assess whether alpha-synuclein was cleared from the brain. Without this, she says, the results cannot conclusively show that plasinezumab is disease-modifying. Vedam-Mai said he would also like to see long-term data to better assess the drug's safety and effectiveness. No serious adverse events occurred in the latest trial.
Researchers could also investigate whether plasinezumab, when taken over a long period of time, is effective for patients with mild Parkinson's disease, Pagano said.
Alzheimer’s disease is a neurological disease that impairs brain functions such as memory and reasoning, and there is currently no known cure. People with this disease begin with basic forgetfulness, gradually lose control of their motor skills, and eventually become unable to complete normal daily activities.
Scientists have discovered that abnormal proteins that accumulate in and around brain cells are the main cause of Alzheimer’s disease. They also discovered that the disease depends on genetics, aging, and lifestyle choices such as being active and eating a healthy diet. However, it is not known how other disorders, such as sleep disorders, may exacerbate symptoms.
Scientists have hypothesized that brain activity during sleep may be related to Alzheimer’s disease because many important memory-related events occur during sleep. Scientists are therefore hoping to find out whether disruptions in brain function during sleep are related to the development of Alzheimer’s disease.
Researchers at Washington University in St. Louis recently tested whether Alzheimer’s disease is related to electrical activity that occurs in the brain during sleep. Most people experience changes in brain activity early in the night as the body relaxes and goes to sleep. Each of these changes sleep vibration event, lasts about 20-40 minutes. The researchers hypothesized that the interactions of brain circuits during sleep oscillations are different in patients with early Alzheimer’s disease and could be used for diagnostic purposes.
To test their hypothesis, the scientists used a machine that measures electrical activity in the brain. electroencephalograph, or brain waves.They chose 205 political partiesParticipants who have previously completed at least 3 nights of EEG measurements, 1 night of home sleep apnea testing, and clinical dementia testing.Based on dementia testing, most One participant had no cognitive impairment, some participants had very mild cognitive impairment, and one participant had mild cognitive impairment.
The researchers asked participants to wear the EEG as a headband while they slept, allowing them to measure brain waves during the sleep oscillation phenomenon. The three types of sleep oscillatory events they measured during the experiment were: theta burst, sleeping spindleand slow waves.
The researchers explained that theta bursts occur when humans are in light sleep and help process information and form memories. Sleep spindles occur during non-rapid eye movement sleep and are involved in memory consolidation. Slow waves occur during deep sleep, slowing heart and breathing rates, and also play a role in memory development.
The researchers categorized each patient’s individual slow-wave events by how often they coincided with sleep spindles and theta bursts. They classified sleep spindle and slow wave events that occur within 1.5 seconds of each other as coupled events. They also classified theta burst and slow wave events that occurred within 0.5 seconds of each other as coupled events.
The researchers found that people with cognitive impairment had weaker electrical activity during theta bursts and greater differences in brain electrical activity during theta bursts and slow waves. They also found that people with cognitive impairment and other biomarkers of Alzheimer’s disease had fewer slow waves with theta bursts and sleep spindles. The researchers interpreted their results to confirm that disruptions in brain circuits involved in memory function during sleep may be associated with Alzheimer’s disease.
The researchers concluded that the EEG pattern of sleep oscillatory events could be used as a biomarker for Alzheimer’s disease. Researchers suggested that early signs of the neurodegenerative process associated with Alzheimer’s disease could be detected in sleeping patients’ brain waves, even before they develop cognitive symptoms. They also believe that the results may provide an accessible and cost-effective tool for monitoring brain health and early Alzheimer’s disease, allowing for earlier responses and improved patient treatment. suggested something.
Alzheimer’s disease is the most common form of dementia, affecting millions of people worldwide. This disease affects the parts of the brain that control memory, thinking, and language. Most commonly, people with Alzheimer’s disease begin to show symptoms. mid 60’s. Scientists have shown that some rare cases of Alzheimer’s disease are caused by a genetic mutation known as PSEN1-E280A, which causes people to develop Alzheimer’s disease as early as their mid-40s, and that this The condition is called early-onset Alzheimer’s disease.
Scientists have identified a Colombian man who carries the gene for early-onset Alzheimer’s disease and a second genetic mutation called the RELN-COLBOS mutation. This man maintained a fully functioning brain for about 30 years longer than the average person with early-onset Alzheimer’s disease. Scientists hypothesized that his genetic mutation could help develop treatments to help others resist Alzheimer’s disease. But additional case studies were needed to find out whether the genetic mutation was the sole reason for the man’s resistance to the disease.
Researchers in Columbia recently set out to study patients with the RELN-COLBOS mutation to see how it may help fight early-onset Alzheimer’s disease. They enrolled the patient in an international collaboration.Antioch University in Columbia and Massachusetts General Hospital in Boston; called Columbia-Boston Biomarker Research Program.This program includes: More than 6,000 participants took part, including those with and without genes known to cause Alzheimer’s disease.
Researchers compared a Colombian man with the RELN-COLBOS mutation to young-onset Alzheimer’s disease patients who do not carry this mutation to determine whether they develop the disease through different pathways. They compared each patient’s cognitive decline in terms of their motor function, number of neurons firing in their brains, and signal strength. They also measured proteins in each patient’s brain that are known to help with memory and learning, such as Dab1 and Tau proteins.
The researchers also collected brain tissue from the man. They performed a type of genetic profiling called. Single cell RNA sequencing Examining his brain tissue revealed that he PSEN1-E280A Gene that causes early-onset Alzheimer’s disease. They used this same method to determine which RELN mutation he had.
They explained that the RELN gene normally tells the body how to make the protein Reelin, which controls brain development.. This man had a mutation in his RELN gene that codes for a different amino acid. Researchers have observed similar mutations in people with other brain-related diseases such as schizophrenia, bipolar disorder, and autism. They named it the RELN-COLBOS mutation, after their research program.
The researchers then looked at the men’s brains using several medical imaging techniques, including positron emission tomography. PET scanmagnetic resonance imaging, or MRI scan. They examined these images of the man’s brain for signs of disease or other abnormalities.
They found that the men’s brains contained large amounts of amyloid beta protein. They explained that this protein causes the loss of neurons and neural connections in Alzheimer’s patients.But the men’s brains were also found to have lower-than-normal levels of another protein called tau protein, which is usually associated with Alzheimer’s disease.. They explained that Alzheimer’s patients typically have high amounts of the protein tau, which disrupts the internal skeleton of neurons and impairs thinking and memory. The researchers suggested that the man’s low levels of tau protein in his brain were part of his resistance to Alzheimer’s disease.
Based on how the RELN-COLBOS mutation acted in this man, scientists hypothesized that it was the cause. Gain-of-function (GOF) mutations. GOF mutations occur when a mutated gene acquires a new function. In other words, it will work differently than it should. For example, a coffee machine’s function is to make coffee, but a GOF mutation could cause it to start making orange juice instead. They classified the RELN-COLBOS mutation as a GOF mutation because the normal function of the RELN gene is to produce the Reelin protein, but the mutant form instead slows down the production of the tau protein.
The researchers concluded that the new function of the RELN-COLBOS mutation may help the gene regulate neural circuits damaged by Alzheimer’s disease and other types of dementia. However, the researchers cautioned that the mutation’s impact on these diseases is modest, as it slows but does not prevent cognitive impairment. They say there are currently only a handful of cases available and that different genetic mutations may delay Alzheimer’s symptoms in the same patient, so future researchers could study other patients with the same mutations. I suggested that it should be done.
Some cancer treatments can cause so-called chemobrain, commonly defined as problems with memory and concentration.
One Bar/Alamy
An experimental treatment for Alzheimer’s disease that involves flickering lights and low-pitched sounds may also help prevent cognitive impairment after cancer treatment, also known as chemical brain, a study in mice suggests.
In the case of Alzheimer’s disease, light and sound stimulation has been shown in small human trials to reduce memory and concentration problems, but larger studies are still investigating it.
The light flashes 40 times per second, or 40 Hz, and the sound also has a frequency of 40 Hz. This frequency was originally chosen because the brainwave intensity of Alzheimer’s patients is lower than 40 Hz and is associated with memory processing. The idea was that this treatment would stimulate these brain waves.
Subsequent research has shown that such brain waves may have a wide range of benefits for the brain, including increased immune cell activity and, more recently, strengthened drainage systems that may help remove a toxic protein called beta-amyloid. It suggests that there is.
Cai Li Hui The Massachusetts Institute of Technology researchers who developed this approach thought it could help cancer patients who have memory and concentration problems after chemotherapy and other cancer treatments. It is thought that these may be caused by damage to brain cells, but the exact mechanism is unknown and there is no cure.
In the latest study, Professor Tsai’s team exposed cancer-free mice to light and sound for one hour a day while being given a common chemotherapy drug called cisplatin, compared to those who had just received chemotherapy. They found that they experienced less decline in mental acuity than mice.
Acuity was assessed by a memory test in which mice were exposed to either new or familiar objects, and the animals typically showed more interest in things they had never seen before. Chemotherapy reduced the mice’s ability to identify objects, but this was prevented by light and sound treatment.
The therapy had several effects, including reducing inflammation in the brain, reducing DNA damage, and reducing the loss of myelin, the insulation around nerve cell fibers.
nazanin derakshan Researchers at Britain’s University of Reading say the idea needs to be tested in people to see if it has any overall benefits. If this treatment is given at the same time as chemotherapy and reduces cell death in the brain, it may help cancer cells survive there, she says.
Cross-section of a mouse brain highlighting neurons that appear to release molecules that increase toxin clearance
Tsai Laboratory/MIT Picower Laboratory
A new explanation has emerged for why an experimental treatment for Alzheimer’s disease that involves flickering sounds and lights may help slow cognitive decline. This frequency appears to strengthen the brain’s waste processing network, helping to remove beta-amyloid and other toxic proteins that contribute to memory and concentration issues.
“Once we understand the mechanism, we can probably understand how to further optimize this whole concept and improve its effectiveness,” he says. Cai Li Hui at Massachusetts Institute of Technology.
The treatment involves exposure to light that flashes at a frequency of 40 times per second, or 40 hertz, and to a bass sound, also at 40 hertz. Typically, stimulation is given for one hour per day.
The key to this new approach is that large networks of brain cells naturally fire in sync with each other at different frequencies, known as brain waves. Brain waves around 40 Hz are common when people are concentrating and forming or accessing memories.
In 2016, Tsai’s team wondered if 40Hz stimulation could enhance cognitive performance in Alzheimer’s patients, since visual or auditory stimulation at a certain frequency is known to enhance brain waves at that same frequency. I decided to investigate.
Their group and other researchers have shown that this reduces amyloid accumulation in mice with Alzheimer’s disease and has cognitive benefits. Small trial in people with this condition, an even larger trial is underway. However, it is unclear how this treatment works, and another idea is that it boosts the function of immune cells in the brain.
Well, the special light and sound appears to work by enhancing the function of the brain’s drainage system, also known as the glymphatic system.
In the latest study, Tsai’s team conducted a series of experiments to study the mechanism of treatment in mice that were genetically modified to have amyloid buildup that normally occurs with age and to have worse memory than typical mice. carried out.
As expected, when the animals were exposed to light and sound, the amount of amyloid decreased. The new findings were that during treatment, the amount of cerebrospinal fluid entering the brain increased, and the amount of waste fluid leaving the brain through the glymphatic vessels increased.
This appears to occur because nearby blood vessels pulsate more, which may help glymph fluid flow through the blood vessels, allowing more water to flow into the glymph system.
The research team also found that the activity of a particular type of brain cell known as an interneuron appears to cause an increase in glymph flow by releasing a molecule called vasoactive intestinal peptide. When the research team chemically blocked the production of this molecule, the treatment no longer accelerated amyloid clearance.
Miken Nedergaard A professor at the University of Rochester in New York who helped discover the glymphatic system says the discovery is consistent with what we already know about it. “The brain, blood, and cerebrospinal fluid are all contained within the skull. When the blood volume expands, the brain tissue cannot be compressed, so the cerebrospinal fluid volume must also move.”
In the accompanying article natural medicineDr. Nedergaard says that a better understanding of the mechanisms of toxin removal in the brain “could be the key to unlocking that.” [their] Treatment Possibilities.”
Crohn’s disease can cause abdominal pain, diarrhea, and weight loss
Jacob Wackerhausen/iStockphoto/Getty Images/www.peopleimages.com
A one-year study of 386 people found that receiving advanced treatment soon after diagnosis of Crohn’s disease improves outcomes for patients.
This disease is a lifelong inflammatory bowel disease; impact millions of peopleIn the world. Symptoms include abdominal pain, diarrhea, fatigue, and weight loss.
“These symptoms have a huge impact on people’s quality of life, education, relationships, and ability to work,” he says. Miles Parks at Cambridge University. “While there is no cure, there are ways to reduce some of these negative outcomes.”
Treatment often includes dietary changes, immunosuppressants, and steroids. In the UK, a drug called infliximab (an antibody that targets a specific protein in the body that is thought to contribute to intestinal inflammation) is given to people who regularly experience flare-ups of Crohn’s disease, or other mild symptoms. It can be prescribed to people who are not responding to. Treatment.
“This is a ‘step-up’ approach where treatment is progressively escalated in a reactive manner as the disease returns,” he says. Nurlaminnuralso at the University of Cambridge.
To see what happens if this more powerful treatment is used as early as possible, Parkes and Noor et al. studied 386 newly diagnosed Crohn’s disease patients aged 16 to 80 in the UK. Recruited people.
They were divided into two groups. One patient received infliximab immediately regardless of symptoms, and the other was treated with other Crohn’s disease drugs. If symptoms persist or continue to worsen, participants in the second group will also be prescribed infliximab, in line with a “step-up” approach.
After one year, 80 percent of patients who initially received infliximab had their symptoms under control over time, compared with only 15 percent of those who did not receive treatment immediately.
Additionally, only 0.5% of people in the group who received infliximab immediately required abdominal surgery for Crohn’s disease, compared to 4.5% in the second group.
The results of this study suggest that giving patients with Crohn’s disease intensive treatment as soon as they are diagnosed may be more effective in improving their lives, Dr. Noor said.
Parks said the extra money spent on medication would be balanced out by not having to pay for subsequent scans, colonoscopies and surgeries for people with repeated relapses.
“People with Crohn’s disease don’t want to be hospitalized or undergo surgery. They want to go out into the outside world and live their lives. Anything that speeds the path to remission. It can only be a good thing,” says Ruth Wakeman of the charity Crohn’s & Colitis UK.
Despite intensive efforts to prevent cardiovascular disease (CVD), substantial residual CVD risk remains, even in people who receive all guideline-recommended interventions. Niacin (vitamin B3) is an essential micronutrient fortified in staple foods, but its role in CVD is poorly understood. Excessive amounts of niacin's breakdown products may be associated with an increased risk of death, heart attack, and stroke, according to a new study.
Niacin is an essential micronutrient that is fortified in staple foods beyond dietary requirements. Image credit: Ferrell other., doi: 10.1038/s41591-023-02793-8.
Although CVD is a major cause of morbidity and mortality worldwide, only a portion of the attributable risk is explained by established risk factors.
Despite significant advances in treatment, the risk of residual cardiovascular disease remains high, and it has been suggested that additional, as yet unrecognized factors contribute to cardiovascular disease.
Research has previously shown that niacin (vitamin B3) reduces levels of low-density lipoprotein cholesterol.
However, this vitamin does not seem to have the expected effect in reducing CVD risk, the so-called “niacin paradox”.
“Our study shows that niacin breakdown products can promote vascular inflammation, providing a potential explanation for this discrepancy,” said Cleveland Clinic researcher Stanley Hazen, Ph.D. said.
In the study, the authors analyzed plasma samples from 4,325 people in three patient cohorts, including men and women from the United States and Europe.
They found that two breakdown products of niacin, the metabolites N1-methyl-2-pyridone-5-carboxamide (2PY) and N1-methyl-4-pyridone-3-carboxamide (4PY), are associated with increased CVD risk. I discovered that
In subsequent human genetic studies and mouse studies, the research team found that this increased risk is due to these breakdown products increasing the abundance of the pro-inflammatory protein VCAM-1 within the endothelial cells lining the blood. showed that it may be mediated by the ability of one of the (4PY). ship.
“Further studies are needed in large-scale studies to investigate the association between niacin and its degradation products and CVD,” the researchers said.
their findings It was published in the magazine natural medicine.
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M. Ferrell other. 2024. End metabolites of niacin promote vascular inflammation and contribute to cardiovascular disease risk. Nat Med 30, 424-434; doi: 10.1038/s41591-023-02793-8
It looked like a classic case of Alzheimer's disease. The man, in his 70s, had been experiencing severe cognitive decline for three years. Frequently forgetting the names of his family members, he was unable to drive or leave the house alone. Further deterioration seemed inevitable. But then his doctor tested him and found that his cerebrospinal fluid sample I noticed a fungus called Cryptococcus neoformans. They put him on antifungal medication and the results were amazing. Within two years he had his driver's license reinstated and returned to his job as a gardener.
Neuroscientists have long suspected that certain infections can increase the risk of dementia.For example, both Porphyromonas gingivalisthe bacteria behind periodontal disease, the herpes simplex virus that causes cold sores, It has been pointed out that there is a relationship with Alzheimer's disease.. However, cases of “reversible dementia” are emerging from the idea that our brains are teeming with microbes and that imbalances in this “brain microbiome” can make people more susceptible to neurodegenerative diseases. is beginning to arouse great interest.
Until recently, it was thought that the brain was free of microorganisms. This was especially due to the blood-brain barrier, a special membrane that protects pathogens and toxins in the blood from the brain. Therefore, the idea of a brain microbiome was controversial. But new research seems to confirm the case. Richard Leeds University of Edinburgh, UK and colleagues Analyzed data obtained from postmortem brains It is housed in four brain banks in the UK and US. They discovered a wide variety of microorganisms of different types.
Chronic obstructive pulmonary disease affects the lungs
Sebastian Kauricki/Science Photo Library
Using inhalable nanoparticles to deliver drugs to the lungs could help treat chronic obstructive pulmonary disease (COPD). In mice with signs of the condition, treatment improved lung function and reduced inflammation.
COPD causes the airways in the lungs to gradually narrow and stiffen, blocking airflow and blocking mucus drainage. As a result, mucus builds up in the lungs, attracting bacterial pathogens that further worsen the disease.
This thick layer of mucus also traps drugs, making it difficult to treat infections. So, Zhu Junliang Researchers at China's Dongzhou University have developed inhalable nanoparticles that can penetrate mucus and deliver drugs deep into the lungs.
The researchers constructed hollow nanoparticles from porous silica and loaded them with an antibiotic called ceftazidime. A shell of negatively charged compounds surrounding the nanoparticles blocked the pores and prevented the antibiotic from leaking. This negative charge also helps the nanoparticles penetrate mucus. The slight acidity of the mucus then changes the charge on the shell from negative to positive, opening the pores and releasing the drug.
Researchers used an inhalation spray containing nanoparticles to treat bacterial lung infections in six mice with signs of COPD. A similar number of animals received antibiotics only.
On average, mice treated with nanoparticles had about 98 percent fewer pathogenic bacteria in their lungs compared to mice given antibiotics alone. They also had fewer inflammatory molecules in their lungs and less carbon dioxide in their blood, indicating better lung function.
These findings suggest that nanoparticles could improve drug delivery to people with COPD and other lung diseases such as cystic fibrosis, where thick mucus makes infections difficult to treat. It has said. vincent rotello from the University of Massachusetts Amherst was not involved in the study. However, it is unclear whether these nanoparticles are cleared from the lungs. “If you have a delivery system that accumulates over time, that's a problem,” he says.
Do not panic! Disease X doesn’t exist yet, but it might someday. Disease The term, coined in 2017, 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 risks of future pandemics at the World Economic Forum’s annual meeting in Davos, Switzerland, this week. “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. That’s because almost everyone in the world now has antibodies to the virus that causes COVID-19, and these appear to offer partial protection against most other pathogens in the coronavirus family. It is.
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 those that can be quickly repurposed 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’s “spike” protein, but can be updated to allow the cells to mass-produce a different protein by simply rewriting the mRNA sequence. there is a possibility.
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 will be. “Disease X is a placeholder,” he says. “You can prepare for any illness.”
Dengue fever is currently endemic in 100 countries, putting half of the world’s population at risk. The threat has increased dramatically, with the number of dengue fever cases increasing tenfold between 2000 and 2019, and the number of cases hitting an all-time high in 2023.
Bangladesh, Peru and Burkina Faso have all seen record outbreaks in the past 12 months, while France, Italy and Spain have also reported cases of mosquito-borne dengue fever.
What’s causing this? Scientists say global warming is making space more hospitable to insects, and that climate change is fueling the rise in this mosquito-borne viral disease. As mosquitoes become more common, we expect the time to outbreak of dengue fever to shorten and the transmission season to lengthen.
This is a worrying situation.But that’s what the sponsoring team decided world mosquito program There is a possible solution. They suggest treating mosquitoes with bacteria that can prevent the development of viruses in the body.
read more:
What are the symptoms of dengue fever?
There’s a good reason dengue fever has been labeled “breakbone fever.” 80% of cases are asymptomatic, but when symptoms develop, symptoms include high fever, muscle and joint pain, severe headache, pain behind the eyes, nausea, and vomiting.
Symptoms begin 4 to 10 days after infection and can last from 2 days to up to a week. DHF (severe dengue fever) manifests as severe abdominal pain, persistent vomiting, bleeding gums or nose, blood in the stool or vomit, pale, cold skin, and fatigue. Doctors can only alleviate these symptoms because antiviral drugs are not available.
How does dengue spread?
Dengue fever is spread through the bite of an infected female mosquito. Aedes aegypti, typically found in tropical and subtropical regions. Originating from the forests of West Africa, Aedes aegypti They spread around the world during the African slave trade and have continued to hitchhike as a means of human transportation ever since.
other Aedes Other species can also transmit dengue fever, although to a lesser extent. The highly invasive Asian tiger mosquito is the likely cause of dengue infections in Europe. Unlike malaria mosquitoes, which usually bite at night and can be prevented with insecticide-treated bed nets, dengue mosquitoes bite during the day and are very difficult to control.
Mosquitoes are now highly urbanized creatures, admirably adapted to coexist with humans, their preferred blood source. In cities, stagnant water is key to survival, providing spawning grounds and habitat for aquatic larval and pupal development. Mosquitoes breed in small puddles in garbage, used tires, and man-made containers such as flower pots. Thus, humans have been the main driving force behind the success of the dengue mosquito.
How can we fight the spread of infection?
Dengue prevention requires a multipronged attack on mosquitoes, with a focus on insecticide spraying. However, insecticide resistance is developing in mosquito populations around the world, threatening their effectiveness.
what else? Control strategies also include adaptations to eliminate breeding sites or prevent reproduction. Aedes aegypti Prevent spawning in stagnant water (remove debris that could trap water and install covers on water storage containers).
Bacterial toxins are also applied to bodies of water to kill mosquito larvae. These strategies are labor intensive because it is difficult to identify, treat, and eliminate all breeding sites. Therefore, new methods of mosquito control are desperately needed.
The World Mosquito Program (WMP) has devised a non-chemical and non-GMO-based approach for dengue control. Bacteria called Wolbachia which occurs naturally in many insect species; Aedes aegypti.
WMP was found to be “infected”. Aedes aegypti and Wolbachia Prevented the onset of dengue virus in adult women. From a logistical point of view, this method is self-sustaining. Wolbachia It can spread to wild populations because it infects eggs through mating.
WMP reports a significant decrease in dengue cases. Aedes aegypti carry Wolbachia has been released.given that Aedes aegypti Since Zika and Chikungunya viruses are also transmitted, WMP has developed a potential “three-for-one” method of disease control.
It’s no exaggeration to say that mosquitoes are the most hated insects, but despite their notoriety, only a handful of the 3,500 species of mosquitoes transmit disease. They are also important to the ecosystem.
Mosquitoes are a food source for fish, frogs, reptiles, bats, and birds, and they are also pollinators, as male insects suck nectar from flowers (only females drink blood). The WMP approach is species-specific and targeted only. Aedes aegyptiThis is in contrast to the “blunt force” approach with insecticides, which can affect insects other than the target.
The climate change trajectory we are currently on is leading to rising temperatures and changing rainfall patterns, which will benefit this terrifying little insect and her viral cargo. Therefore, we need as many weapons as possible in our arsenal to combat the growing global dengue threat.
Researchers have discovered a unique case in a Colombian family where a woman with a genetic predisposition to Alzheimer’s disease remained cognitively healthy due to a rare APOE gene mutation, the Christchurch mutation. This mutation disrupts the typical progression of Alzheimer’s disease and suggests new prevention strategies. Dementia may be prevented by breaking the link between early and late stages of the disease.
The disease has plagued one large Colombian family for generations, killing half of them in their prime years. But one member of the family avoided what seemed like fate. She remained cognitively healthy well into her 70s, even though her relatives inherited her genetic defect that caused her to develop dementia in her 40s.
Researchers at Washington University School of Medicine in St. Louis now think they know why. Previous research had reported that the woman was in possession of two copies of the rare variant, unlike her relatives. Apoe A gene known as the Christchurch mutation.
In this study, researchers used genetically modified mice to show that the Christchurch mutation was associated with early stages of Alzheimer’s disease, when a protein called amyloid beta accumulates in the brain, and another protein called tau, which causes cognitive impairment. begins to decline. So the women remained mentally alert for decades, even though their brains were filled with large amounts of amyloid.
“All protective factors are very interesting because they give us new clues about how the disease works,” said lead authors Barbara Barton, Ph.D., and Reuben M. said David M. Holzman, M.D., Morris III Professor Emeritus of Neurology.
Understanding the progression of Alzheimer’s disease, the researches found thatthe main difference was the level of activity of microglia, the brain’s waste-processing cells. Microglia tend to cluster around amyloid plaques. In mice with Apoe The Christchurch mutation activated microglia surrounding amyloid plaques, making them highly efficient at consuming and processing tau aggregates.
Reference: “APOE3ch alters microglial responses and suppresses Aβ-induced tau dissemination and spread” Yun Chen, Sihui Song, Samira Parhizkar, Jennifer Lord, Yiyang Zhu, Michael R. Strickland, Chanung Wang, Jiyu Park, G By Travis Tabor, Hong Jiang, Kevin Lee, Albert A. Davis, Carla M. Huede, Marco Colonna, Jason D. Ulrich, David M. Holtzman, December 11, 2023. cell.DOI: 10.1016/j.cell.2023.11.029
Researchers have discovered a way to detect Parkinson’s disease up to 30 years before symptoms appear using biomarkers and PET scans. This breakthrough includes tracking neurodegeneration more sensitively than current methods and shows that rapid eye movement sleep behavior disorder (RBD) is an important early indicator of Parkinson’s disease. is identified. This discovery could lead to earlier diagnosis and treatment, potentially up to 10 years earlier than currently.
Researchers at The Florey and Austin Health in Melbourne, Australia, have demonstrated the potential to identify early indicators of Parkinson’s disease 20 to 30 years before the onset of symptoms. This breakthrough paves the way for early screening programs and intervention, potentially allowing treatment before significant damage occurs.
Researchers at the Florey Institute and Austin Health have demonstrated the possibility of identifying early indicators of Parkinson’s disease 20 to 30 years before the onset of symptoms. This breakthrough paves the way for early screening efforts and preventive treatment, long before permanent damage occurs.
Florey Professor Kevin Burnham said that although Parkinson’s disease, a debilitating neurodegenerative disease, is often thought of as a disease of the elderly, it actually begins in midlife and can last for decades. He said it may not be detected.
“Parkinson’s disease is very difficult to diagnose until symptoms become apparent, by which time up to 85 percent of the neurons in the brain that control motor coordination have been destroyed. At that point, many treatments are likely to be ineffective,” Professor Burnham said. “Our long-term goal is to find ways to detect diseases earlier and treat people before they cause harm.”
Advanced diagnostic technology
In a recently published study, neurologylead researcher Professor Burnham and colleagues explore how a known biomarker called F-AV-133 can be used in positron emission tomography (PET) scans to diagnose Parkinson’s disease and accurately track neurodegeneration. I’m explaining how it can be done.
In the Melbourne study, Austin Health’s Frawley Professor Chris Rowe and his team studied 26 patients with Parkinson’s disease, 12 controls, and 11 patients with rapid eye movement sleep behavior disorder (RBD), a strong indicator of Parkinson’s disease. I checked the name. .
Each person underwent two PET scans two years apart. Key findings include:
Currently available assessments of Parkinson’s disease showed no significant changes in clinical symptoms in any of the participants.
In contrast, PET scans showed “significant neuronal loss” in three key areas of the brains of people with the disease, making F-AV-133 more effective than what is currently available. also suggests that it is a sensitive means of monitoring neurodegeneration.
Further mathematical modeling yields the following calculation:
Slow nerve cell loss over a total of approximately 33 years in Parkinson’s disease
This loss takes about 10.5 years before the disease is detected on a PET scan.
Even if a PET scan detects the disease, it will take another six and a half years for motor symptoms to appear.
It takes about 3 years after physical symptoms appear until a clinical diagnosis is confirmed.
This corresponds to approximately 22.5 years of neuronal loss before clinical symptoms are sufficient for diagnosis.
Professor Burnham said the findings pave the way for the development of screening protocols to diagnose and treat Parkinson’s disease up to 10 years earlier than is currently possible. It may also help identify patients for clinical trials.
What is RBD?
RBD stands for Rapid Eye Movement Behavior Disorder.
Patients with RBD scream, thrash, and sometimes move violently during sleep, enacting vivid and disturbing dreams.
RBD is caused by a lack of muscle relaxation (sleep paralysis).
90% of RBD patients develop Parkinson’s disease.
Half of all Parkinson’s patients have RBD.
RBD is an important warning sign for early Parkinson’s disease.
If you have RBD, see a sleep specialist or neurologist.
Reference: “Use of 18F-AV-133 VMAT2 PET Imaging to Monitor Progressive Nigrostriatal Degeneration in Parkinson’s Disease”, Leah C. Beauchamp, Vincent Dore, Victor L. Villemagne, SanSan Xu, David Finkelstein, Kevin J. Barnham, Christopher Rowe, 28 November 2023 neurology. DOI: 10.1212/WNL.0000000000207748
A recent study presented at the 2023 American Heart Association’s Scientific Sessions highlighted the link between mental health and cardiovascular disease. The study found that anxiety and depression can hasten the onset of cardiovascular risk factors, that cumulative stress scores are significantly associated with heart disease, and that mental health has a significant impact on heart health.
Two other studies presented at the same session also linked mental health and heart health, showing that depression and anxiety may accelerate the development of cardiovascular risk factors and critical events. According to one study conducted in Boston, people with a higher genetic susceptibility to stress developed cardiovascular risk factors at a younger age than those without the genetic marker. A separate Dallas-based study found that accumulated stress contributes to negative health behaviors such as smoking, leading to worsened cardiovascular health.
The American Heart Association emphasizes that mental health conditions such as depression, anxiety, and stress increase the risk of poor heart health. Two new studies have found that a person’s mental state may affect their health to a greater extent than previously thought.
One study examined the mechanisms by which mental state affects heart health, finding that depression and anxiety accelerate the development of new cardiovascular risk factors. Researchers found that people with depression or anxiety developed new risk factors on average six months earlier than those without mental health conditions, and were at a higher risk for major cardiovascular events. Another study showed that cumulative stress scores were significantly associated with increased risks of atherosclerosis and overall cardiovascular disease.
Researchers encouraged more frequent screenings for cardiovascular risk factors in people with depression and anxiety, and suggested that treatment for these mental health conditions may reduce the acceleration of cardiovascular risk factors.
The two studies presented at the 2023 American Heart Association Scientific Sessions underscore the interdependence of mental and heart health, and emphasize the need for proactive care for mental health conditions in order to improve overall heart health.
A groundbreaking study proves that Alzheimer’s disease symptoms can be induced in healthy animals through gut microbiome transmission, highlighting the gut-brain connection and suggesting early treatment and treatment of Alzheimer’s disease. New avenues for personalized interventions have been opened.
Researchers have discovered a link between the gut microbiome and gut bacteria. Alzheimer’s disease disease.
For the first time, research has demonstrated that symptoms of Alzheimer’s disease can be transmitted to healthy young organisms through the gut microbiome, confirming its role in Alzheimer’s disease.
The research was led by Professor Yvonne Nolan from APC Microbiome Ireland, the world’s leading SFI-funded research center based at University College Cork (UCC), and Professor Yvonne Nolan from UCC’s Department of Anatomy and Neuroscience. Professor Sandrine Thure, King’s College London, and Dr. Annamaria Cattaneo, IRCCS Fatebenefratelli, Italy.
Scientists have discovered a link between Alzheimer’s disease and the gut microbiome. Pictured are Dr. Stephanie Grabracer and Professor Yvonne Nolan. Credit: UGC
This study confirms that the gut microbiome is emerging as an important research target for Alzheimer’s disease, given its sensitivity to lifestyle and environmental influences.
was announced on brainThis study shows that memory impairment in Alzheimer’s patients can be transferred to younger animals through gut microbiota transplantation.
Alzheimer’s disease, memory impairment, gut microbiome
Patients with Alzheimer’s disease had greater abundance of pro-inflammatory bacteria in their fecal samples, and these changes were directly correlated with the patients’ cognitive status.
Professor Yvonne Nolan said: “The memory test we investigated relies on the growth of new neurons in the hippocampal region of the brain. Animals with the gut bacteria of Alzheimer’s patients produced fewer new neurons and had impaired memory. I found out that it is true.”
“Alzheimer’s patients are typically diagnosed at or after the onset of cognitive symptoms, which may be too late, at least with current treatments. “Understanding the role of gut bacteria could pave the way for the development of new treatments and even personalized interventions,” Professor Nolan said.
Implications for treatment strategies and research collaborations
Alzheimer’s disease is the most common cause of dementia and is a general term for memory loss and other cognitive impairments severe enough to interfere with daily life. As the population ages, one in three people born today could develop Alzheimer’s disease. Funded by Science Foundation Ireland, scientists at UCC are leading the way in healthy brain aging by investigating how the gut microbiome responds to lifestyle influences such as diet and exercise. We are working to develop strategies to accelerate and advance the treatment of Alzheimer’s disease.
Professor Sandrine Thuret, Professor of Neuroscience at King’s College London and one of the study’s senior authors, said: ‘Alzheimer’s disease is an insidious disease and there is still no effective treatment. , represents an important advance in the understanding of this disease, confirming that the composition of our gut microbiota is causally linked to the development of the disease. This collaboration will help future research in this field. We hope that this will lead to potential advances in therapeutic interventions.”
Professor. John F. Cryan, vice president of research and innovation at UCC, who also worked on the study, said: He conducts research into related diseases such as Alzheimer’s disease, and with UCC he recognizes APC Microbiome Ireland as a leading institution in microbiome and brain health research. This research is consistent with our UCC Futures Framework and the University’s strategic plans in the areas of food, microbiome, health and, soon to be launched, Future Aging and Brain Sciences. “
Reference: “The microbiota of Alzheimer’s patients induces defects in cognition and hippocampal neurogenesis” Stephanie Grubrucker, Moira Marizzoni, Edina Silajzic, Nicola Lopizzo, Elisa Mombelli, Sarah Nicolas, Sebastian Dom-Hansen, Katia Scacellati, Davide Vito Moretti, Melissa Rosa, Carina Hoffman, John F. Cryan, Olivia F. O’Leary, Jane A. English, Aongus Lovell, Cora O’Neill, Sandrine. Ture, Annamaria Cattaneo, Yvonne M. Nolan, October 18, 2023; brain. DOI: 10.1093/brain/awad303
The research was carried out by Dr Stephanie Grubrucker, a postdoctoral researcher in collaboration with Professor Nolan, in collaboration with postdoctoral colleagues Dr Edina Siladzic from King’s College London and Dr Moira Marizzoni from IRCCS Fatebenefratelli in Italy. It was carried out. UCC collaborators were Professor Cora O’Neill, Dr Olivia O’Leary, Dr Sarah Nicholas, Dr Jane English, Mr Sebastian Dohm Hansen and Dr Aongus Lovell.
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