Promising New Method for Eliminating Brain Waste in Alzheimer’s Disease

Posted on April 6, 2026 by Igor Mitreski

Scanning electron micrograph of mouse nerve cells affected by misfolded amyloid and beta proteins, believed to cause Alzheimer’s disease.

Linnea Lundgren/Linear Imaging/Science Photo Library

Scanning electron micrograph of mouse nerve cells affected by misfolded amyloid and beta proteins, implicated in Alzheimer's disease. — Scanning electron micrograph of mouse nerve cells affected by misfolded amyloid and beta proteins, believed to cause Alzheimer’s disease.

Linnea Lundgren/Linear Imaging/Science Photo Library

Research is increasingly focused on utilizing the brain’s waste disposal system to potentially slow or mitigate Alzheimer’s disease. A recent technique has demonstrated success in removing toxic protein aggregates associated with Alzheimer’s from mouse brains, leading to improved memory and learning test results.

This technique targets a receptor known as DDR2, traditionally associated with lung health. “Inhibiting the DDR2 pathway could theoretically decrease amyloid beta protein levels while simultaneously enhancing waste removal,” explains Jia Li from Guangzhou Medical University, China. “We are optimistic that we can ultimately reverse Alzheimer’s disease.”

The buildup of misfolded proteins, such as amyloid plaques and tau tangles in the brain, is considered a primary trigger for Alzheimer’s. While existing medications can remove amyloid aggregates, they often do not significantly alleviate symptoms. Thus, research is shifting towards innovative strategies, including enhancing the glymphatic system responsible for waste clearance in the brain.

Lee and colleagues plan to further investigate receptors in cell membranes that may boost glymphatic function as one of their roles. DDR2, studied extensively for its role in pulmonary fibrosis, is also implicated in Alzheimer’s disease by Jinsu and his team at Guangzhou Medical University. Pulmonary fibrosis occurs when the extracellular matrix surrounding cells fails, leading to excessive collagen deposition and oxygen supply limitations.

Research indicates that the malfunctioning extracellular matrix is associated with amyloid and tau proteins in Alzheimer’s disease. “This restriction of oxygen can hinder cognitive functions like thinking and memory,” states Lee.

To explore DDR2’s role, the researchers reviewed human tissue databases and discovered DDR2’s scarcity. However, they found substantial amounts in brain samples from Alzheimer’s patients. “We confirmed that DDR2 is prevalent in Alzheimer’s disease brain tissue for the first time,” notes Su.

Through various experiments in human and primate cells, along with mouse models, researchers propose that DDR2 regulates the cellular dysfunction responsible for the disease’s symptoms. This is substantiated by findings that three cell types increase DDR2 in their membranes during Alzheimer’s: reactive astrocytes, surrounding amyloid beta masses; perivascular fibroblasts, which alter activity prior to Alzheimer’s onset; and choroid plexus epithelial cells that are crucial for cerebrospinal fluid production, essential for the glymphatic system.

These findings suggest that targeting DDR2 could impact multiple facets of Alzheimer’s simultaneously, as noted by Siju Gu from Harvard University. Yet, due to the complexity of the condition, he remains cautious about potential reversibility of Alzheimer’s disease.

The researchers developed a monoclonal antibody aimed at blocking the DDR2 receptor. In mouse models of Alzheimer’s, this intervention improved spatial learning and memory, alongside reduced DDR2 levels, fewer amyloid plaques, and enhanced glymphatic activity.

“The mouse model results are promising and highlight the role of glymphatic function and cerebrospinal fluid dynamics in brain health,” Gu remarked. “This suggests DDR2 could be a viable target for Alzheimer’s disease therapies.”

Cesar Cunha from Denmark’s Novo Nordisk Foundation Center for Basic Metabolic Research expressed appreciation for the researchers’ focus on more than just amyloid plaques, noting their model relates to a rare inherited form of Alzheimer’s that typically arises earlier. Its applicability to the more common late-onset Alzheimer’s remains uncertain.

Professor Hsu, however, indicates that DDR2 upregulation occurs in both familial and late-onset Alzheimer’s, suggesting the treatment has potential widespread efficacy. DDR2 expression appears to increase with age, a factor alongside hypoxia, both recognized risk factors for late-onset Alzheimer’s.

Currently, researchers are embarking on clinical trials that use tracers to monitor DDR2 levels in Alzheimer’s patients’ brains, aiming to determine the antibodies’ delivery paths. They are also developing smaller antibodies to facilitate more efficient crossing of the blood-brain barrier.

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Source: www.newscientist.com

Boosting Vitamin D in Midlife Linked to Reduced Alzheimer’s Disease Biomarkers Later

Posted on April 3, 2026 by Igor Mitreski

In a groundbreaking study, Dr. Martin David Mulligan from the University of Galway and his team investigated the long-term effects of vitamin D levels on brain health by following nearly 800 participants from the Framingham Heart Study for over 15 years. Their findings revealed that individuals with higher circulating levels of vitamin D at age 30 exhibited significantly less accumulation of tau protein—a key factor in the development of Alzheimer’s disease—when retested approximately 16 years later. This association remained robust even after accounting for various factors such as age, gender, cardiovascular health, smoking, depression, and BMI.

Vitamin D deficiency in midlife may be a modifiable risk factor for preclinical dementia signs observed in neuroimaging. Image credit: Aloysio Costa Latoje.

Dementia currently ranks as a leading cause of morbidity worldwide, impacting an estimated 57 million individuals.

“Our research indicates that maintaining high vitamin D levels during midlife may safeguard against the formation of tau deposits in the brain, while insufficient vitamin D could serve as a modifiable risk factor for dementia,” stated Dr. Mulligan.

“Further validation through additional studies is essential to confirm these results.”

The study analyzed data from 793 adults (53% female, average age 39 years) who were dementia-free at the time of brain imaging.

Blood levels of 25-hydroxyvitamin D were measured between 2002 and 2005, followed by positron emission tomography (PET) scans assessing tau and amyloid deposits conducted from 2016 to 2019.

Accumulation of tau protein, particularly in regions like the entorhinal cortex and temporal lobe, is known to play a crucial role in the early onset of Alzheimer’s disease.

Researchers observed that elevated vitamin D levels correlated with reduced tau levels throughout the brain and in these vulnerable areas.

“Notably, 34% of participants exhibited low vitamin D levels, and only 5% were taking vitamin D supplements,” the researchers reported.

This study contributes to the growing body of evidence correlating vitamin D with brain health, focusing specifically on early preclinical changes rather than solely on clinical outcomes like dementia diagnosis and aging.

Scientists propose that ensuring adequate vitamin D levels in midlife may serve as a proactive strategy to mitigate neurodegenerative changes before clinical symptoms manifest.

However, it is important to note that this study does not establish a direct causal relationship between vitamin D and the prevention of tau accumulation or dementia. The researchers measured vitamin D at a single time point without tracking its changes over the years, and they did not assess whether supplementation influenced brain health.

“These promising findings suggest a significant association between increased vitamin D levels in early midlife and decreased tau load 16 years later,” Dr. Mulligan remarked.

“Midlife is a critical phase where modifying risk factors could yield substantial benefits.”

For more information, refer to the published results in the journal Neurology.

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Martin David Mulligan et al. 2026. Association of circulating vitamin D in midlife with increased tau-PET burden in adults without dementia. Neurology 2 (2): e000057; doi: 10.1212/WN9.0000000000000057

Source: www.sci.news

Enhancing the Brain’s Cleansing System to Combat Alzheimer’s Proteins

Posted on March 25, 2026 by Igor Mitreski

The glymphatic system facilitates the removal of brain waste products.

Klaus Renau/Science Photo Library

Diagram illustrating the glymphatic system, the brain's waste clearance network. — The glymphatic system facilitates the removal of brain waste products.

Klaus Renau/Science Photo Library

Researchers have discovered a groundbreaking drug that enhances the brain’s waste disposal system, effectively eliminating proteins linked to Alzheimer’s disease. A sedative commonly used in medical settings, when paired with a blood pressure stabilizer, shows promise in safely and efficiently clearing these toxic proteins, potentially delaying the disease’s onset by up to seven years.

“This is a significant advancement,” states Siju Gu from Harvard University, who was not part of the study. “While it may benefit individuals with neurodegenerative disorders, it could also enhance brain function in healthy individuals.”

The brain utilizes the glymphatic system, a vital network of channels surrounding blood vessels, to eliminate metabolic waste, directing it into the lymphatic system for blood disposal. This system is most active during deep sleep stages, wherein slow brain waves facilitate waste removal. However, its efficiency declines with age, especially in Alzheimer’s disease.

Previous research revealed that dexmedetomidine, a sedative widely used during procedures, boosts brain wave activity in mice. This enhancement improves the brain’s waste elimination capacity and slows cognitive decline in Alzheimer’s mouse models.

To assess dexmedetomidine’s effects in humans, Paul Dagham and his team at Applied Cognition, a pharmaceutical firm in California, enlisted 19 adults averaging 60 years of age. After a night of sleep deprivation in a controlled environment, blood samples were collected for baseline measurements.

Participants then received a four-hour infusion of dexmedetomidine alongside midodrine, a medication that mitigates low blood pressure, a common side effect of the sedative. Following a nap, additional blood samples were collected.

This experiment was replicated a few weeks later, with participants receiving a placebo and saline instead. The resulting analysis revealed that the combination of dexmedetomidine and midodrine, dubbed ACX-02, effectively removed amyloid and tau proteins—two proteins predisposed to misfolding and aggregation—better than the placebo treatment.

Dagham estimates that if ACX-02’s effects persist for several years, it could defer Alzheimer’s disease onset or progression by about seven years based on typical misfolded amyloid levels in those at risk. “This could significantly impact individuals at risk,” a research team member noted, including Jeff Iliff from the University of Washington.

Further analysis indicates that ACX-02 enhances the number of slow brain waves during sleep transitions and increases cerebral fluid flow, accelerating waste removal. Moreover, blood vessels appear to dilate and contract more effectively, enabling better fluid propulsion through the glymphatic system.

Though antibody therapies targeting amyloid plaques, such as lecanemab and donanemab, have received approval in the US and UK, their efficacy on symptoms remains minimal and they may cause hemorrhaging and swelling in the brain. “Innovative treatments are urgently needed. We know that the antibodies for Alzheimer’s are ineffective and can induce serious side effects,” asserts Natalie Beth Corner from the German Center for Neurodegenerative Diseases in Bonn.

No severe side effects were noted in Iliff’s trial. By enhancing the glymphatic system, there is less activation of the brain’s immune cells compared to antibody treatments, reducing risk factors associated with side effects, Dagham explains. ACX-02 additionally targets both amyloid beta and tau, which could augment its cognitive benefits. The research team plans to explore this further in patients with early Alzheimer’s disease.

Dr. Gu recognized that prior attempts to eliminate misfolded amyloid beta and tau in Alzheimer’s patients yielded limited success. However, he emphasized that if this novel approach proves safe and effective, it could see widespread application. “It may also benefit individuals with other neurodegenerative disorders linked to protein misfolding, such as Parkinson’s disease,” he states. Iliff adds that developing dexmedetomidine tablets could help treat diminished alertness due to sleep deprivation.

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Source: www.newscientist.com

How to Reduce Inflammation and Lower Your Risk of Alzheimer’s Disease

Posted on March 6, 2026 by Igor Mitreski

Unforeseen vaccine side effects: Staying sharp is a bonus!

Joseph Polc / Alamy

Recent studies indicate that chronic inflammation in various body areas could contribute to Alzheimer’s disease. While it may take time to fully understand these connections, it’s evident that persistent inflammation has adverse effects and that reducing it can provide numerous health benefits.

Inflammation is the body’s response when immune activity exceeds normal levels, such as when a wound becomes infected. While short-term inflammation is beneficial, prolonged inflammation can lead to serious health issues, including cancer, heart disease, stroke, rheumatoid arthritis, and mental health disorders like depression and anxiety.

To combat long-term inflammation and enhance both physical and mental health, consider the following tips:

1. Get Vaccinated

Vaccines, including those for shingles, tuberculosis, and influenza, have demonstrated a reduced risk of dementia. For instance, individuals who received the Shingrix vaccine experienced a 17% lower chance of developing dementia compared to those who had the older Zostavax vaccine, which also lowers dementia risk. Though the exact mechanism remains unclear, vaccines likely reduce inflammation.

2. Maintain Good Oral Hygiene

Gum disease is another inflammatory condition linked to an increased risk of Alzheimer’s and heart disease. Bleeding gums can allow harmful bacteria to enter the bloodstream, which is why good dental hygiene is essential for preventing periodontal disease and maintaining overall health.

3. Embrace a Mediterranean Diet

A Mediterranean diet is rich in anti-inflammatory foods such as fruits, beans, nuts, whole grains, fish, and olive oil, while minimizing inflammatory foods like red and processed meats. This dietary approach not only helps in reducing inflammation but is also associated with longevity and overall wellness.

4. Exercise Regularly

Sedentary lifestyles contribute to increased inflammation. Numerous studies suggest that regular exercise diminishes inflammation. Whether it’s vigorous workouts or gentler activities like yoga, incorporating movement into your routine can provide significant health benefits.

5. Achieve a Healthy Weight

Although the connection is still being explored, obesity is often linked to ongoing inflammation. It raises an interesting question: Could medications like GLP-1, often used for weight loss, reduce Alzheimer’s risk? Current evidence shows that those using GLP-1 medications may experience lower dementia risk, but results for those without diabetes are still unclear.

6. Cultivate Happiness

While occasional stress is normal, chronic stress can lead to inflammation. Striving for happiness and emotional balance can help mitigate inflammation and improve overall mental well-being.

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Source: www.newscientist.com

How Skin, Lung, and Intestinal Inflammation Could Signal Early Onset of Alzheimer’s Disease

Posted on March 5, 2026 by Igor Mitreski

Amyloid plaques in the brain are a defining feature of Alzheimer’s disease, but what if the roots of the condition start elsewhere in the body?

Alamy

Alzheimer’s disease has traditionally been believed to originate in the brain. However, comprehensive genomic analysis indicates that inflammation in distant organs such as the skin, lungs, or intestines may initiate the condition, potentially decades before noticeable memory decline occurs. This shift in understanding could shed light on why Alzheimer’s treatments have been largely ineffective. Current drugs intervene too late; a focus on early-stage inflammation in peripheral organs may be crucial.

“As neuroscientists, we tend to focus on the brain, but this study highlights that the brain is interconnected with the body, and changes elsewhere can impact brain function,” states Donna Wilcock from Indiana University, not involved in the study. “Although Alzheimer’s is a brain disorder, we must consider the entire body when discussing its genesis.”

To explore the genetic underpinnings of Alzheimer’s disease, researchers including Cesar Cunha from Denmark’s Novo Nordisk Foundation Basic Metabolic Research Center analyzed genetic data from the European Alzheimer’s and Dementia Biobank, encompassing over 85,000 individuals with the disease and approximately 485,000 without it. They also evaluated gene activity in 5 million single cells across 40 body regions and 100 brain regions.

The study scrutinized 1,000 genes linked to an increased Alzheimer’s disease risk, surprisingly finding these genes were more abundant in organs like the skin, lungs, and digestive system than in the brain. “It was counterintuitive at first because the expression of these risk genes in brain cells seemed low,” notes Cunha. “Our continued analysis revealed their primary presence in other body parts.”

Many of these Alzheimer’s risk genes are tied to immune regulation and are particularly abundant in barrier tissues like the skin and lungs, which defend against bacteria and toxins through inflammatory responses. “This suggests that Alzheimer’s might initiate due to inflammation in these peripheral organs,” Cunha explains. Genetic variations may even dictate the extent of inflammation and its impact on brain health. Hence, individuals with a family history of Alzheimer’s could be more vulnerable to the disease amidst infections or inflammatory episodes.

Interestingly, the highest expression of these gene variants occurs when individuals reach ages 55 to 60. Inflammation during this period seems likely to trigger Alzheimer’s, corroborated by long-term studies from Hawaii. Inflammatory markers rise in individuals in their late 50s, with those in their 70s and 80s exhibiting increased Alzheimer’s likelihood. “A person could suffer from lung inflammation due to a viral infection at age 55, which might initiate Alzheimer’s 30 years later, but the exact mechanisms remain elusive,” Cunha remarks.

Rezanur Rahman, a researcher at QIMR Berghofer Medical Research Institute, has identified a genetic mutation associated with Alzheimer’s that appears concentrated in the skin and lungs. More research is essential to understand their functional role in symptom progression, Rahman states. “Association does not imply causation.”

Nonetheless, findings imply that individuals with various inflammatory conditions—such as eczema, cold sores, pneumonia, periodontal disease, Lyme disease, syphilis, diabetes, high blood pressure, and intestinal infections—may face heightened Alzheimer’s disease risk in the future. This correlation is particularly robust when inflammation occurs in middle age, around ages 45 to 60, aligning with Cunha’s insights.

Previously, the brain was deemed immune-privileged and largely unaffected by inflammatory processes elsewhere in the body. Bryce Vissel from St. Vincent’s Hospital in Sydney, Australia, among those who first proposed inflammation as a trigger for Alzheimer’s, acknowledges that while initially contentious, new evidence supports that peripheral inflammation from infections or injuries may indeed instigate the disease.Infection or injury can affect brain function.

When inflammation occurs, immune cells are activated, releasing signaling proteins like cytokines that can cross into the brain via the bloodstream. An unpublished study by Vissel and his team indicates that cytokines may disrupt neuronal connections, potentially leading to memory impairment.

Concurrently, research has shown that the blood-brain barrier becomes more permeable with age, allowing inflammatory cytokines and immune cells easier access, which might elucidate why inflammation poses more of a risk during mid-life compared to youth, Cunha notes.

Current theories posit that Alzheimer’s disease stems from the accumulation of misfolded beta-amyloid and tau proteins within the brain. Yet, treatments aimed at eliminating these proteins have yielded minimal success, indicating that such accumulation might be a symptom rather than the core issue. “We’ve been trying to treat the result of the disease, not its cause,” Cunha argues.

Cunha likens this to past mistakes in obesity treatments, which initially targeted excess fat directly, failing until genetic research revealed that mutations connected with obesity are often highly expressed in the brain, disrupting appetite and energy balance. This led to the development of the weight-loss medication semaglutide (marketed as Ozempic and Wegovy), which modulates brain pathways to curb appetite.

If Alzheimer’s originates from peripheral inflammation, its treatment would necessitate a paradigm shift, Cunha asserts. Data indicate that midlife vaccinations may offer protective benefits against Alzheimer’s disease. A recent Californian study revealed that adults receiving both doses of the shingles vaccine recommended for individuals aged 50 and older were 50% less likely to develop Alzheimer’s by age 65. Another investigation found that those aged 50 and older treated with the Bacillus Calmette-Guérin (BCG) vaccine for bladder cancer had a 20% reduced risk of onset.

This phenomenon might arise as vaccines bolster the aging immune system and mitigate inflammation, suggests Wilcock. “At age 55, we should invigorate our immune systems and remind them to stay active, as most vaccinations occur in childhood.”

Beyond vaccinations, several lifestyle interventions have been shown to diminish inflammation and avert Alzheimer’s disease. These include adopting a Mediterranean diet, limiting alcohol consumption, exercising, quitting smoking, and managing blood pressure and cholesterol levels.

Professor Cunha emphasizes that the challenge lies in convincing fellow neuroscientists to recognize peripheral inflammation as a potential contributor to Alzheimer’s disease. “I’ve encountered skepticism at academic conferences, being told, ‘If you aren’t focusing on amyloid, you’re not studying Alzheimer’s disease,'” he shares. “After decades entrenched in amyloid research, adapting one’s perspective can be daunting.”

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Source: www.newscientist.com

Understanding Why Alzheimer’s Disease-Related Brain Damage Doesn’t Immediately Trigger Symptoms

Posted on January 30, 2026 by Igor Mitreski

Examining Resilience to Alzheimer’s Disease: Why Some Individuals Remain Symptom-Free

Associated Press/Alamy

Recent studies reveal that some individuals exhibit brain changes tied to Alzheimer’s disease yet show no symptoms like memory loss. Though the reasons remain unclear, innovative research is uncovering protective factors that may prevent cognitive decline.

Alzheimer’s disease is marked by amyloid plaques and tau tangles accumulating in the brain, widely believed to contribute to cognitive decline. However, some individuals, known for their resilience, defy this notion. In 2022, Henne Holstege and her team at the University Medical Center in Amsterdam discovered that certain centenarians retain good cognitive function despite these pathological changes.

Expanding on this research, the team conducted a new study involving 190 deceased individuals. Among them, 88 had Alzheimer’s diagnoses, while 53 showed no signs of the disease at death. Their ages ranged from 50 to 99, and 49 were centenarians with no dementia, though 18 exhibited cognitive impairment previously.

The focus was on the middle temporal gyrus—an early site of amyloid plaques and tau tangles in Alzheimer’s. Interestingly, centenarians with elevated amyloid levels had tau levels akin to those without Alzheimer’s, suggesting that limiting tau accumulation is critical for resilience, according to Holstege.

While amyloid plaques are linked to cognitive decline, Holstege posits that tau accumulation may activate a cascade of symptoms. Notably, amyloid plaques alone may not cause significant tau tangling. “Without amyloid, tau can’t spread,” she explains.

Further analysis of approximately 3,500 brain proteins revealed only five were significantly associated with high amyloid plaques, while nearly 670 correlated with tau tangles. Many of these proteins are involved in crucial metabolic processes like cell growth and waste clearance. Holstege emphasizes, “With amyloid, everything changes; with tau, it’s a different story.”

In the cohort of 18 centenarians with high amyloid levels, 13 showed significant tau spread throughout the middle temporal gyrus, a pattern similar to Alzheimer’s, but the overall tau presence remained low.

This distinction is vital, as diagnosis hinges on tau spread, indicating that accumulation, not just proliferation, triggers cognitive decline. “We must understand that proliferation doesn’t mean abundance,” Holstege clarifies.

In a second study, Katherine Prater and her team at the University of Washington examined 33 deceased individuals—10 diagnosed with Alzheimer’s, 10 showing no signs, and 13 deemed resilient. Most subjects were over 80 and underwent cognitive assessments within a year before death.

In line with previous findings, the research indicated that tau was present but not accumulated in resilient brains. Though the mechanisms remain elusive, Prater theorizes that microglia—immune cells regulating brain inflammation—might play a crucial role in maintaining cognitive function in resilience.

Previous research has shown that microglia often become dysfunctional in Alzheimer’s disease, contributing to degenerative processes. While the researchers could not analyze microglia extensively, Holstege noted their significance.

The team also conducted genetic studies on microglia from the dorsolateral prefrontal cortex, essential for managing complex tasks. They discovered that resilient individuals’ microglia exhibited heightened activity in messenger RNA transport genes compared to those with Alzheimer’s. This suggests effective gene transport, vital for protein synthesis, is preserved in resilient brains.

“Disruptions in this process can severely impact cell function,” Dr. Prater remarked at the Neuroscience Society meeting in San Diego. However, its direct relationship to Alzheimer’s resilience remains to be elucidated.

Moreover, resilient microglia demonstrated reduced activity in metabolic energy genes compared to those in Alzheimer’s patients, mirroring patterns in healthy individuals. This suggests heightened energy expenditure in Alzheimer’s due to inflammatory states that disrupt neuronal connections and lead to cell death.

“Both studies indicate that the human brain possesses mechanisms to mitigate tau burdens,” Prater concludes. Insights gained from this research could pave the way for new interventions to delay or even prevent Alzheimer’s disease. “While we aren’t close to a cure, the biology offers hope,” she stated.

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Brain/
Alzheimer’s Disease

Source: www.newscientist.com

Gene Removal Reverses Alzheimer’s Disease in Mice: Breakthrough Findings from Sciworthy

Posted on January 8, 2026 by Igor Mitreski

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.

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Source: sciworthy.com

New Study Unveils Breakthrough Approach for Alzheimer’s Disease Recovery by Targeting Cellular Energy Deficits

Posted on December 31, 2025 by Igor Mitreski

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

Source: www.sci.news

Walking 3,000 Steps Daily Could Help Slow Alzheimer’s Disease Decline

Posted on November 3, 2025 by

Gentle exercises, like walking, can enhance brain health

Gordon Scammell/Loop Images/Universal Images Group via Getty Images

SEI 272889769 — Gentle exercises, like walking, can enhance brain health

Gordon Scammell/Loop Images/Universal Images Group via Getty Images

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.

Topics:

exercise/
Alzheimer’s disease

Source: www.newscientist.com

Initiating HRT During Early Menopause Could Lower Alzheimer’s Risk in Women

Posted on September 19, 2025 by Igor Mitreski

A decrease in estrogen during menopause may affect cognitive function

Elena Popova/Getty Images

Commencing hormone replacement therapy (HRT) within five years of the onset of postmenopause appears to decrease the likelihood of developing Alzheimer’s disease. In contrast, starting HRT later in life may have adverse effects, indicating that the timing of the therapy is crucial for its impact on the brain.

Women face a greater risk of developing Alzheimer’s, particularly after menopause, compared to men. This heightened risk may be linked to reduced estrogen levels, which play vital roles in brain energy regulation and inflammation. Consequently, HRT has surfaced as a potential method to reduce Alzheimer’s risk following menopause. However, research on its effectiveness has produced mixed outcomes.

To investigate this, Fnu Vaibhav Pandit Bagwat Deira Sharma from Health Science University in India and his team analyzed 53 studies encompassing over 8.4 million postmenopausal participants regarding Alzheimer’s disease prevalence.

In a randomized controlled trial, participants receiving HRT exhibited, on average, a 38% greater risk of developing Alzheimer’s compared to those not on HRT. Conversely, observational studies suggested a 22% reduction in Alzheimer’s risk among HRT users.

Vaibhav presented these findings at a meeting with the American Nerve Association in Maryland on September 15th, noting that the disparity is likely age-related. Most subjects in the randomized trial were over 65, while those in observational studies tended to be younger. Further analysis revealed that individuals who initiated HRT within five years post-menopause had a decreased risk of Alzheimer’s by 32% over a follow-up period ranging from five years to others that consumed their lifetime.

“This transition during menopause represents a neurological shift,” stated Roberta Brinton from the University of Arizona, who was not part of the research. As estrogen levels decline, the brain seeks alternative energy sources. There is some evidence suggesting that this reallocation may utilize compounds meant for brain function while sacrificing others, leading to potential neurodegeneration. She posits that HRT may either initiate or halt this transition during menopause. However, if the brain has already undergone this shift, HRT may be ineffective.

“More research is essential to clarify this perplexity,” remarked Vaibhav. Without a clearer comprehension of HRT’s impact, he warns that “women may miss out on advantages, and some may inadvertently face harm.”

topic:

Source: www.newscientist.com

Researchers are creating digital self-assessment tools for diagnosing Alzheimer’s disease.

Posted on September 15, 2025 by Igor Mitreski

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

Source: www.sci.news

Omega Fatty Acids May Help Safeguard Women Against Alzheimer’s Disease

Posted on August 21, 2025 by Igor Mitreski

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

Source: www.sci.news

Low-Dose Lithium Alleviates Alzheimer’s Symptoms in Mice

Posted on August 6, 2025 by Igor Mitreski

Illustration of neurons affected by Alzheimer’s disease

Science Photo Library / Alamy Stock Photo

Illustration of neurons impacted by Alzheimer's Disease — Illustration of neurons affected by Alzheimer’s disease

Science Photo Library / Alamy Stock Photo

Research indicates that administering lithium to mice with low brain levels reverses cognitive decline associated with Alzheimer’s disease. These findings imply that lithium deficiency could contribute to Alzheimer’s, and low-dose lithium treatments may have therapeutic potential.

Several studies have highlighted a relationship between lithium and Alzheimer’s. A 2022 study found that individuals prescribed lithium faced nearly half the risk of developing Alzheimer’s. Another paper published recently linked lithium levels in drinking water with a reduced risk of dementia.

However, as Bruce Yankner from Harvard University points out, hidden variables may influence these results. He suggests that other elements in drinking water, like magnesium, might also contribute to a lower dementia risk.

Yankner and his team assessed metal levels in the brains of 285 deceased individuals, 94 of whom had Alzheimer’s, and 58 exhibited mild cognitive impairment. The remaining participants showed no cognitive decline prior to death.

They discovered that lithium concentrations in the prefrontal cortex (a vital area for memory and decision-making) were about 36% lower in those without cognitive decline, and 23% lower in individuals with mild cognitive impairment. “I believe environmental factors, including diet and genetics, play a significant role,” states Yankner.

There’s another concerning aspect. In Alzheimer’s patients, amyloid plaques exhibited nearly three times more lithium than areas without plaques. “Lithium is sequestered by these plaques,” explains Yankner. “Initially, there’s a lithium intake disorder, and as the disease advances, lithium levels decline further due to its binding to amyloid.”

To further investigate cognitive effects, the research team genetically modified 22 mice to mimic Alzheimer’s symptoms and reduced their lithium consumption by 92%. After around eight months, these mice performed significantly worse on various memory assessments compared to 16 mice on normal diets. For instance, even after six days of training, lithium-deficient mice took approximately 10 seconds longer to locate a hidden platform in a water maze. Their brains also had about 2.5 times more amyloid plaques.

Genetic evaluations of brain cells from the lithium-deficient mice indicated heightened activity of genes linked to neurodegeneration and Alzheimer’s. These mice experienced increased encephalopathy, and their immune cells failed to eliminate amyloid plaques, mirroring changes seen in Alzheimer’s patients.

The researchers then evaluated various lithium compounds for their ability to bind with amyloid and found that orotium— a compound created through the combination of lithium and orotic acid— had the least propensity to be trapped in plaques. A nine-month treatment regimen with orotium significantly diminished amyloid plaques in Alzheimer’s-like mice and improved memory performance compared to regular mice.

These findings point toward the potential of lithium orotium as a treatment for Alzheimer’s. High doses of various lithium salts are already being employed to manage conditions such as bipolar disorder. “A significant challenge with lithium treatment in the elderly is the risk of kidney and thyroid toxicity due to high dosages,” notes Yankner. However, he mentions that the quantities used in this study were about 1,000 times lower than those typically administered, which may account for the absence of kidney or thyroid issues observed in the mice.

Nonetheless, clinical trials are crucial to gauge how low doses of orotium lithium might impact humans, says Rudolf Tansy at Massachusetts General Hospital. “The challenge lies in determining who truly requires lithium,” he adds. “Excessive lithium intake can result in severe side effects.”

Topics:

Source: www.newscientist.com

Could Cancer Medications Pave the Way for Alzheimer’s Treatment?

Posted on July 21, 2025 by Igor Mitreski

As treatment options for Alzheimer’s disease remain limited, researchers are exploring the repurposing of cancer medications to address cognitive decline.

The incidence of Alzheimer’s is on the rise due to an aging global population, yet no cure currently exists. Efforts to discover new therapies that can halt the progression of the disease instead of merely managing symptoms have often been unsuccessful.

At present, only two medications, Leqembi and Kisunla, have received FDA approval to slow the progression of early Alzheimer’s disease, and the extent of their effectiveness is considered limited.

Several pharmaceutical firms have either shelved or discontinued their Alzheimer’s drug development initiatives after encountering trial failures. Others are investigating the potential of established medications, including popular weight loss drugs in combating the disease.

In this context, researchers at the University of California, San Francisco, conducted extensive screenings of existing drugs that could be repurposed for Alzheimer’s treatment, aiming to shorten the time required for patient access to these drugs. They analyzed a database of over 1,300 different medications, spanning various drug classes such as antipsychotics, antibiotics, antifungals, and chemotherapeutics, and assessed their impact on gene expression.

Their recent study, published in the journal Cell, pinpointed two cancer drugs as the leading candidates to potentially mitigate the risk of Alzheimer’s in patients. When used in combination, these drugs demonstrated the ability to slow or even reverse Alzheimer’s symptoms in mouse models. One of the medications is typically used for breast cancer treatment, while the other targets colon and lung cancers.

Significant alterations in gene expression in the brain are characteristic of Alzheimer’s disease, leading to the increased synthesis of certain proteins and decreased production of others. These disruptions can impair brain functionality and result in symptoms such as memory loss.

According to the researchers, the two drugs, identified from a database of nearly 90, were able to reverse the expression of genes associated with Alzheimer’s in human brain cells. Furthermore, based on electronic medical records, five specific drugs appeared to lower Alzheimer’s risk among actual patients, ultimately leading the authors to select two FDA-approved cancer treatments for animal testing.

“We were not anticipating that cancer medications would emerge as strong contenders,” remarked Marina Sirota, interim director of the UCSF Bakar Computational Health Sciences Institute.

The authors noted that letrozole, a breast cancer treatment, seems to modify gene expression within neurons, while irinotecan, a colon cancer medication, appears to influence gene expression in glial cells that support the nervous system. Alzheimer’s disease leads to nerve cell destruction, excess glial cell proliferation, and brain inflammation.

A 2020 study indicated that breast cancer patients treated with letrozole had a lower incidence of Alzheimer’s disease compared to those who did not receive the drug. Similarly, colorectal cancer survivors who were administered irinotecan exhibited a reduced risk of Alzheimer’s disease, as noted in research from 2021.

After evaluating the drugs in mice, the study authors discovered that the combination of the two medications reversed cognitive decline and enhanced memory in mice displaying traits of Alzheimer’s disease as they aged.

Given that results observed in mice do not always have a direct correlation with human outcomes, researchers aim to conduct clinical trials with Alzheimer’s patients.

“The development of new medications typically incurs costs in the millions, often billions, and can span over a decade. In contrast, repurposed medications may require only two to three years and carry significantly lower costs to reach clinical trial stages,” Sirota explained.

“Currently, we are not producing highly effective treatments that can significantly decelerate cognitive decline,” she added.

The challenge in developing Alzheimer’s treatments lies in the intricate nature of the disease, with its exact causes remaining largely elusive.

At this point, the authors admit that the precise mechanisms by which cancer drugs may be effective against Alzheimer’s are uncertain. One hypothesis suggests that breast cancer medications inhibit estrogen production—a hormone that regulates the expression of numerous genes. Colon cancer drugs might mitigate brain inflammation by preventing glial cell proliferation, yet Huang notes that there could be additional explanations.

Dr. Melanie McReynolds, a biochemistry assistant professor at Penn State University who was not involved in the research, offered another perspective.

She suggested that the study indicates various cancer drugs may prove beneficial in treating Alzheimer’s by modulating glucose metabolism, the process by which cells generate energy. McReynolds emphasized that this process is vital for communication among different brain cells.

“Aging, stress, and illness can disrupt that communication,” she stated.

McReynolds expressed that the drug combinations evaluated in the current research have the potential to reverse metabolic declines.

However, it is crucial to understand how Alzheimer’s patients will respond to these cancer drug combinations. Letrozole can induce hot flashes, while irinotecan is known for causing severe diarrhea. Both treatments may also lead to nausea and vomiting.

“These medications come with significant side effects, so it’s essential to weigh these risks carefully and determine whether such side effects are manageable for individuals with Alzheimer’s,” stated Sirota. “It’s not a straightforward solution.”

Source: www.nbcnews.com

The Use of Music by Neuroscientists in Treating Alzheimer’s Disease and other ailments

Posted on January 7, 2025 by Igor Mitreski

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…

Source: www.newscientist.com

Possible Future Solutions for Slowing, Stopping, or Eradicating Alzheimer’s Disease

Posted on September 2, 2024 by Igor Mitreski

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.

Source: www.newscientist.com

A revolutionary anti-aging vaccine offers hope in preventing diseases like Alzheimer’s

Posted on July 3, 2024 by Igor Mitreski

I’ll be 60 in just over 5 years, which is a big deal. I already have an age-related disease (high blood pressure), and the odds are good that I haven’t been diagnosed with at least one more by then. After that, the symptoms of age will pile up and bring me to my inevitable end. Many of you will no doubt be in a similar situation. We are living longer than ever before, but those extra years don’t necessarily come with good health.

But judging by recent trends, my sons may be even luckier. Instead of facing a long list of common diseases in their 70s and 80s, they may be able to immunize themselves against them. They may be able to celebrate middle age with vaccinations that immunize them against Alzheimer’s, cancer, and hypertension. What’s more, they may even have access to an anti-aging panacea that vaccinates against all of these and more, allowing them to enter old age in better health than most of us today could hope to achieve.

Suddenly, an ancient medical technique looks set to become a game changer in the fight against diseases associated with age. Vaccines, the most commonly used injections for infectious diseases like COVID-19 and measles, are now showing promise for treating non-infectious diseases, particularly those associated with age. The field is advancing rapidly, and there are signs that, in the right winds, I and others my age might be able to benefit from these vaccinations. It’s so…

Source: www.newscientist.com

Researcher working on promising Alzheimer’s drug facing charges of research fraud

Posted on June 29, 2024 by Igor Mitreski

Summary

A neuroscientist who helped develop a potential treatment for Alzheimer’s disease has been indicted on fraud charges.
The charges relate to allegations that the scientists fabricated research images and data that they may have used to win grant funding.
Manipulation of research images is a growing concern in the scientific community.

A neuroscientist who contributed to the development of a potential Alzheimer’s disease treatment is facing fraud charges after a federal grand jury indictment on Thursday.

The indictment alleges that Wang Huaoyang, a professor of medicine at the City University of New York, engaged in fraudulent activities, including falsifying research images and data to secure grant funding from the National Institutes of Health.

Wang worked with Cassava Sciences, a pharmaceutical company based in Austin, Texas, on the development of simufilam, a drug candidate for Alzheimer’s disease. The indictment states that Wang received around $16 million in grant funding from Cassava for early-stage drug development.

The indictment accuses Wang of fraud against the United States, wire fraud, and making false statements. It claims that Wang manipulated images of Western blots, a laboratory technique used to detect proteins, to support his research and grant applications.

The indictment also suggests that Wang provided false information to scientific journals to support his research on symphyllum, a drug currently in late-stage clinical trials.

Despite the charges, Wang did not respond to requests for comment. His research has faced scrutiny in the past, leading to retractions of multiple studies and an investigation by CUNY.

Cassava Sciences confirmed that Wang was not involved in their latest clinical trials and emphasized that his research focused on early-stage drug development.

The scientific community has expressed growing concerns about research misconduct and the manipulation of data and images. Instances of research misconduct, such as the allegations against Wang, have led to retractions of studies and raised questions about the integrity of scientific research.

CUNY has stated that they will cooperate fully with the federal investigation into Wang’s alleged misconduct until the matter is resolved. The university acknowledges the seriousness of the charges and the impact they may have on the scientific community.

The case highlights the importance of maintaining integrity and transparency in scientific research to ensure the credibility and validity of scientific discoveries.

Retraction Watch has reported on the retraction of several academic papers authored by Wang, further underscoring the need for accountability and ethical practices in scientific research.

Source: www.nbcnews.com

Colombian family genetics may reveal secret to delaying Alzheimer’s disease

Posted on June 20, 2024 by Igor Mitreski

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.

Source: www.nbcnews.com

Brain activity during sleep linked to Alzheimer’s disease, say researchers

Posted on March 12, 2024 by Igor Mitreski

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.

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Source: sciworthy.com

Delaying Alzheimer’s Disease with a Genetic Mutation

Posted on March 11, 2024 by Igor Mitreski

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.

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Source: sciworthy.com

Light and sound therapy may provide preventative measures against chemically-induced brain changes in Alzheimer’s disease

Posted on March 7, 2024 by Igor Mitreski

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.

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Source: www.newscientist.com

Slowing Alzheimer’s Disease Progression: How Light and Sound Can Remove Toxins from the Brain

Posted on February 28, 2024 by Igor Mitreski

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.”

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Source: www.newscientist.com

The Crucial Link Between the Brain Microbiome and Curing Alzheimer’s Disease

Posted on February 19, 2024 by Igor Mitreski

Russell Kightley/Science Photo Library

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.

Source: www.newscientist.com

A Unique Patient Mutation Offers New Hope for Preventing Alzheimer’s Disease

Posted on December 25, 2023 by Igor Mitreski

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

Source: scitechdaily.com

Scientists at Stanford University identify shared genetic factor that offers protection against Alzheimer’s and Parkinson’s diseases

Posted on December 11, 2023 by Igor Mitreski

Stanford Medicine and international collaborators have discovered that around 20% of individuals carry genetic mutations that reduce their risk of Alzheimer’s disease or Parkinson’s disease by 10% or more. This particular variant, known as DR4, has the potential to enhance future vaccines for these neurodegenerative diseases. In addition, the study found a potential link between the tau protein and both diseases, providing new possibilities for targeted therapies and vaccines.

The large-scale analysis included medical and genetic information from a wide range of individuals across different continents. This data analysis revealed that certain gene variants related to immune function are associated with a lower risk of developing Alzheimer’s and Parkinson’s diseases. Approximately one in five people possess a specific genetic mutation that provides resistance to both diseases.

The research, led by Stanford Medicine, indicates that individuals with this protective genetic mutation may be less likely to benefit from future vaccines aimed at slowing or stopping the progression of these common neurodegenerative diseases. Results from the analysis of medical and genetic data from hundreds of thousands of people from diverse backgrounds confirmed that carrying the DR4 allele increased the average chance of developing Parkinson’s or Alzheimer’s disease by more than 10%. New evidence has also surfaced suggesting that the tau protein, which is known for aggregating in the brains of Alzheimer’s patients, may also play a role in the development of Parkinson’s disease.

The study, published in the Proceedings of the National Academy of Sciences, was a collaboration between researchers at Stanford Medicine and international partners. The researchers involved in this study were Emmanuel Mignot, MD, Michael Gracius, MD, Iqbal Farooq, and Asad Jamal from Stanford Medicine, as well as Dr. Jean-Charles Lambert from Inserm, University of Lille, France. The lead author was Yan Le Nguyen, Ph.D., and other contributors included Dr. Guo Luo, Dr. Aditya Ambati, and Dr. Vincent Damot.

Further findings from the study showed that individuals with the DR4 allele were more likely to develop neurofibrillary tangles, characteristic of Alzheimer’s disease, in their brains. The study also suggests that tau, a protein central to Alzheimer’s disease, may have an unknown role in Parkinson’s disease.

DR4 is a particular allele of the DRB1 gene, which is a part of the human lymphocyte antigen complex. This complex is crucial in allowing the immune system to recognize the internal contents of cells. One of the significant findings of this study was that the specific peptide fragment that DR4 recognizes and presents is a chemically modified segment of the tau protein, which plays a role in both diseases. The study suggests that the DR4 allele could be used to create a vaccine targeting this modified peptide as a potential way to interfere with tau aggregation and the development of these neurodegenerative diseases. There may be potential to delay or slow the progression of the diseases in individuals who carry the protective variants of DR4.

The study also noted that the effectiveness of the vaccine may depend on the subtype of DR4 a person carries, which varies among different ethnic groups. For example, one subtype of DR4 that is more common among East Asians may be less protective against neurodegenerative diseases.

Source: scitechdaily.com

The microbiome may be linked to memory loss in Alzheimer’s disease, new study finds

Posted on November 12, 2023 by Igor Mitreski

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.

Source: scitechdaily.com

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Tag Archives: Alzheimers

Promising New Method for Eliminating Brain Waste in Alzheimer’s Disease

Boosting Vitamin D in Midlife Linked to Reduced Alzheimer’s Disease Biomarkers Later

Enhancing the Brain’s Cleansing System to Combat Alzheimer’s Proteins

How to Reduce Inflammation and Lower Your Risk of Alzheimer’s Disease

1. Get Vaccinated

2. Maintain Good Oral Hygiene

3. Embrace a Mediterranean Diet

4. Exercise Regularly

5. Achieve a Healthy Weight

6. Cultivate Happiness

How Skin, Lung, and Intestinal Inflammation Could Signal Early Onset of Alzheimer’s Disease

Understanding Why Alzheimer’s Disease-Related Brain Damage Doesn’t Immediately Trigger Symptoms

Gene Removal Reverses Alzheimer’s Disease in Mice: Breakthrough Findings from Sciworthy

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Summary

Colombian family genetics may reveal secret to delaying Alzheimer’s disease

Brain activity during sleep linked to Alzheimer’s disease, say researchers

Delaying Alzheimer’s Disease with a Genetic Mutation

Light and sound therapy may provide preventative measures against chemically-induced brain changes in Alzheimer’s disease

Slowing Alzheimer’s Disease Progression: How Light and Sound Can Remove Toxins from the Brain

The Crucial Link Between the Brain Microbiome and Curing Alzheimer’s Disease

A Unique Patient Mutation Offers New Hope for Preventing Alzheimer’s Disease

Scientists at Stanford University identify shared genetic factor that offers protection against Alzheimer’s and Parkinson’s diseases

The microbiome may be linked to memory loss in Alzheimer’s disease, new study finds

Alzheimer’s disease, memory impairment, gut microbiome

Implications for treatment strategies and research collaborations