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Alzheimer's

Episodes

vitamin d

Why Vitamin D Deficiency Accelerates Brain Aging

Posted on May 13th 2025 (7 days)

Dr. Rhonda Patrick discusses a study that found vitamin D supplementation was associated with a 40% lower risk of dementia.

alcohol

The Truth About Alcohol: Risks, Benefits, and Everything In-Between | Dr. Rhonda Patrick

Posted on June 27th 2024 (11 months)

In this episode, we’re taking a deep dive into alcohol. We’ll explore the science, misconceptions, controversies, and health effects of this widely used drug.

rhonda
Premium

Q&A #59 with Dr. Rhonda Patrick (5/11/24)

Posted on May 31st 2024 (12 months)

Dr. Rhonda Patrick discusses resistant starch, red light therapy risks, stem cells, and the link between benzodiazepines and dementia in her latest Q&A session.

Topic Pages

  • Alcohol

    Alcohol is one of the most widely used and abused drugs and is associated with several health conditions.

  • Blood-brain barrier

    The blood-brain barrier allows the passage of nutrients and cell signals from the bloodstream to the brain while excluding harmful substances.

  • Brain-derived neurotrophic factor (BDNF)

    BDNF is a growth factor known for its influence on neuronal health and for its role in mediating the beneficial cognitive effects associated with exercise.

  • Choline

    Choline is an essential nutrient critical for various bodily functions, including brain development, liver health, and muscle function.

  • Melatonin

    Melatonin is a hormone involved in the sleep-wake cycle that might also have benefits for neurodegenerative diseases like Alzheimer's and dementia.

  • Polyphenol-rich diets and neurodegeneration (glycemic control)
    stub

    Polphenol-rich diets promote better glucose regulation can help slow brain aging, preserve hippocampal function, and reduce cognitive decline over time.

  • Resveratrol

    Resveratrol is a polyphenolic compound produced in plants that demonstrates anti-inflammatory and anti-aging properties in humans.

  • Salmon roe

    Salmon roe, the internal egg mass found in female salmon, is rich in protein, vitamins, and the omega-3 fatty acids EPA and DHA.

  • Sauna

    Sauna use exposes the body to extreme heat and, in turn, induces protective responses that improve health and may increase healthspan.

  • Small vessel disease

    Small vessel disease is a generic term that describes dysfunction of blood vessels that occurs with aging and contributes to cognitive decline, cardiovascular disease, frailty, and stroke.

News & Publications

  • A modified Mediterranean ketogenic diet boosts healthy brain fats and reduces Alzheimer's-associated markers, suggesting potential neuroprotective effects. pmc.ncbi.nlm.nih.gov
    Nutrition Brain Alzheimer's Diet Ketogenic Diet

    Roughly 60% of the human brain is made up of fat, which plays a crucial role in the structure and function of brain cells. In Alzheimer’s, fat metabolism in the brain becomes altered, influencing disease progression. A recent study found that a modified Mediterranean ketogenic diet boosted healthy fats in the brain and lowered Alzheimer’s-associated markers.

    The study included 20 adults with prediabetes who were at risk for developing Alzheimer’s. Participants followed the modified Mediterranean ketogenic diet or the American Heart Association diet for six weeks. After a six-week break, they switched to the opposite diet for another six weeks. Before and after each diet intervention, participants underwent cognitive testing, and the researchers evaluated their blood lipids and Alzheimer’s markers, including amyloid-beta and tau.

    They found that the modified Mediterranean ketogenic diet caused notable changes in blood lipids, increasing molecules linked to fat breakdown and energy use (such as free fatty acids and acylcarnitines) while lowering triglycerides. It also boosted healthy lipid types (plasmalogens) and reduced harmful ones (deoxyceramides). These alterations in blood lipids correlated with improved Alzheimer’s biomarkers and cognitive measures. The American Heart Association diet had little or no effect on blood lipids or cognitive function.

    The traditional ketogenic diet is high in fat and low in carbohydrates. The modified Mediterranean-ketogenic diet is rich in fish, lean meats, and fiber-rich green leafy vegetables, nuts, and berries. About 5% to 10% of its calories come from carbohydrates, 60% to 65% from fat, and 30% from protein. In the American Heart Association diet, about 55% to 65% of calories come from carbohydrates, 15% to 20% from fat, and 20% to 30% from protein.

    The findings from this small intervention study suggest that a modified Mediterranean ketogenic diet protects against Alzheimer’s disease. Learn more about the ketogenic diet and Alzheimer’s disease in this clip featuring Dr. Dale Bredesen.

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  • Traumatic brain injuries reactivate dormant herpes simplex virus, causing inflammation and accumulation of harmful proteins in the brain, a process potentially linked to Alzheimer's disease. www.science.org
    Brain Alzheimer's Inflammation Virus TBI

    Each year, millions of people sustain a traumatic brain injury (TBI), often resulting in serious, long-term consequences. Research indicates that even one head injury is linked to a higher risk of developing dementia, with the risk increasing further after two or more. A recent study found that TBIs can reactivate dormant herpes simplex virus type 1 (HSV-1), driving neuroinflammation and contributing to the development of Alzheimer’s.

    Researchers created a three-dimensional model of the human brain. Then, they subjected HSV-1-infected and non-infected brain tissue to multiple blows, emulating TBIs and their ensuing pro-inflammatory effects.

    They found that repeated mild blows to HSV-1-infected tissues reactivated the virus, triggering inflammatory processes in the brain and driving the buildup of amyloid-beta and phosphorylated tau—proteins linked to brain damage and memory loss. These harmful effects worsened with additional injuries but didn’t occur in uninfected tissue.

    These findings demonstrate that viral reactivation in the brain may contribute to the development of Alzheimer’s. HSV-1 is the virus responsible for causing cold sores and genital herpes. It infects approximately 80% of people by age 60 and is commonly found in the brains of older adults. In people with the APOE4 gene, HSV-1 markedly increases the risk of Alzheimer’s.

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  • A nasal spray delivering stem cell-derived extracellular vesicles reduces inflammation and improves brain function in a mouse model of Alzheimer's disease. isevjournals.onlinelibrary.wiley.com
    Brain Alzheimer's Inflammation Stem Cells Memory

    Stem cell-based therapies show promise as treatments for neurodegenerative diseases, including Alzheimer’s. However, transplanting stem cells into the brain carries considerable risks. A recent study found that a nasal spray that delivered neural stem cell extracellular vesicles—tiny particles that carry proteins and genetic material—reduced inflammation and improved brain function in a mouse model of Alzheimer’s disease, offering a safer, less risky approach.

    Researchers used neural stem cell-derived extracellular vesicles created from induced pluripotent stem cells. They administered the vesicles via nasal spray to three-month-old Alzheimer’s model mice. Then, they tracked the vesicles' interaction with brain cells, focusing on microglia and astrocytes, and analyzed gene activity, brain pathology, and behavioral changes.

    They found that the vesicles reduced inflammatory activity in brain cells, decreased levels of amyloid-beta plaques and phosphorylated tau (hallmarks of Alzheimer’s), and improved memory and mood in the mice. These effects persisted for at least two months after treatment without impairing the brain’s immune processes and protein clearance.

    These findings suggest that a nasal spray containing stem cell-derived extracellular vesicles offers a promising new therapy for Alzheimer’s disease, targeting inflammation and preserving brain function while avoiding the risks of direct stem cell transplantation. Other research demonstrates the effectiveness of stem cell therapies for eye diseases. Learn more in this clip featuring Dr. David Sinclair.

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  • Smoking accelerates cognitive decline by 17% over a decade. www.eurekalert.org
    Exercise Alzheimer's Alcohol Dementia

    Smoking has numerous harmful effects on health, including increased risks of lung cancer, heart disease, and stroke. Evidence indicates smoking also contributes to cognitive decline, affecting memory and fluency. A recent study found that smoking accelerates cognitive decline by as much as 17% over time.

    Researchers examined data from more than 32,000 cognitively healthy adults aged 50 to 104 from 14 European countries. They grouped participants according to whether they smoked, engaged in regular exercise, were socially active, and drank moderately—defined as less than or equal to two alcoholic drinks per day for men or one drink per day for women. Then, they analyzed the effects of lifestyle on memory and fluency decline over 10 years.

    They found that non-smokers maintained relatively stable memory and fluency scores over the 10 years. However, smokers experienced up to 17 percent greater decline in memory and up to 16 percent greater decline in fluency, even after considering other factors that influence cognitive aging, including age at baseline, gender, country, education, wealth, and chronic conditions. Interestingly, healthy lifestyle behaviors offset some of the risks associated with smoking, with smokers who exercised, socialized, and drank moderately exhibiting cognitive declines comparable to non-smokers.

    These findings suggest that smoking markedly increases cognitive decline, increasing the risk for Alzheimer’s disease and other forms of dementia. Quitting smoking can be challenging, but mindfulness techniques can help. Learn more about mindfulness in this clip featuring Dr. Ashley Mason.

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  • Chronic inflammation in early adulthood can impair cognitive performance by midlife, with 39% of young adults showing high inflammation levels. pubmed.ncbi.nlm.nih.gov
    Brain Alzheimer's Aging Inflammation Memory Dementia

    Research demonstrates that inflammation in later life harms the brain, increasing the risk of dementia and cognitive decline. However, scientists don’t fully understand the effects of inflammation that begins in early adulthood. A recent study found that inflammation during early adulthood markedly impairs cognitive performance in midlife.

    The research involved more than 2,300 young adults (aged 24 to 58) enrolled in the Coronary Artery Risk Development in Young Adults study. Researchers tracked the participants' inflammation levels, measured by C-reactive protein (CRP), for about 18 years. Five years after their last CRP measurement, the participants completed tests that measured their verbal memory, processing speed, executive function, verbal fluency, category fluency, and overall cognition.

    The researchers identified three inflammation patterns among the participants: lower stable (45%), moderate/increasing (16%), and consistently higher (39%). Participants with consistently higher CRP levels were 67 percent more likely to experience poor processing speed and 36 percent more likely to have poor executive function than those with stable, low CRP levels. Those with moderate/increasing CRP levels were twice as likely to have poor processing speed. There were no significant associations between CRP levels and memory, verbal fluency, category fluency, or overall cognition.

    One of the many ways inflammation harms the brain is through its effects on pericytes, tiny cells that surround the brain’s blood vessels and help maintain the blood-brain barrier. Inflammation causes pericytes to release pro-inflammatory cytokines, compromising the barrier and facilitating neurodegeneration. Learn more about links between inflammation, pericytes, and cognitive decline in this clip featuring Dr. Axel Montagne.

    These findings indicate that more than one-third of young adults have high inflammation levels, adversely affecting executive function and processing speed by midlife. They also underscore the importance of managing inflammation throughout life. Omega-3 fatty acids have potent anti-inflammatory effects. Learn more in this episode featuring Dr. Bill Harris.

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  • Multivitamin/mineral supplements enhance memory and cognitive function in older adults, a finding from the COSMOS trial. www.sciencedirect.com
    Brain Alzheimer's Aging Micronutrients Dementia

    As the global population ages, the number of people at risk for Alzheimer’s disease and other forms of dementia increases. A robust and growing body of evidence indicates that lifestyle influences the risk of developing dementia. A recent study found that multivitamin/mineral supplements improve memory and slow cognitive aging in older adults – roughly equivalent to reducing cognitive aging by two years.

    Researchers investigated the effects of multivitamin/mineral supplementation on cognitive function in a subset of participants enrolled in the COSMOS study, a randomized, double-blind, placebo-controlled trial involving more than 21,000 older adults (60 years or older) in the U.S. Participants in COSMOS were randomly assigned to receive one of three interventions: cocoa extract (providing 500 milligrams of flavanols daily, including 80 milligrams of epicatechin), a multivitamin/mineral supplement, or both, daily for two years. A fourth group received a placebo. In the subset, called COSMOS-Clinic, 573 participants underwent extensive brain function tests before and after the study and again two years later.

    They found that multivitamin/mineral supplementation conferred modest improvements in overall cognitive function over two years in participants enrolled in the subset, particularly in episodic memory – the ability to recall specific events, experiences, and contextual details from one’s past. They did not observe improvements in the participants' executive function or attention. However, a meta-analysis involving more than 5,000 participants from the COSMOS-Clinic, COSMOS-Mind, and COSMOS-Web studies demonstrated that multivitamin/mineral supplementation markedly improved overall cognition and episodic memory.

    These findings from the COSMOS trials suggest that multivitamin/mineral supplementation – a low-cost, low-effort intervention – improves cognitive function in older adults. They also highlight the role of adequate nutrition throughout the lifespan and support the “micronutrient triage theory” – the idea that the body prioritizes the utilization of micronutrients for metabolic pathways needed for survival and reproduction over those used for long-term health. Learn more about micronutrient triage theory in this clip featuring Dr. Bruce Ames.

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  • Poor oral health may triple Alzheimer's disease risk. www.brainandlife.org
    Alzheimer's Dementia Dental

    Oral health is intricately linked to overall well-being, with emerging research identifying associations between poor oral health and an increased risk of many chronic diseases, including cardiovascular disease, diabetes, and cancer. A recent study found that oral diseases associated with tooth loss more than tripled the risk of developing Alzheimer’s disease.

    Researchers assessed Alzheimer’s disease risk among more than 32 million people. They categorized the participants as having normal or poor oral health and assessed serum biomarkers associated with Alzheimer’s, including blood glucose, lipids, and C-reactive protein (a marker of inflammation).

    They found that more than 1.2 million participants had poor oral health, while the remainder had normal oral health. Those with poor oral health were more than twice as likely to develop Alzheimer’s disease than those with normal oral health, regardless of age, gender, or serum biomarkers. Those with oral conditions associated with tooth loss were more than three times more likely to develop Alzheimer’s.

    The findings from this large epidemiological study suggest that poor oral health markedly increases a person’s risk for developing Alzheimer’s disease. In vitro research further supports these findings, demonstrating that oral bacteria colonize the brain and release toxins that disrupt the blood-brain barrier, impairing its function and increasing the risk of Alzheimer’s. And research in mice shows that oral bacteria over-stimulate microglia, impairing their ability to eliminate amyloid-beta, a harmful protein linked to Alzheimer’s.

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  • Dementia cases could surpass previous estimates by 40 percent, highlighting the need for prevention. medicalxpress.com
    Alzheimer's Aging Dementia

    Nearly 50 million people worldwide live with Alzheimer’s disease or another form of dementia — a number projected to triple in the coming decades. However, a recent study suggests the number could be even higher, as much as 40 percent more than previous estimates.

    Researchers analyzed data from the English Longitudinal Study of Ageing, a long-term study of older adults living in England and Wales. They identified dementia cases from among more than 90,000 people. Then, they analyzed how dementia incidence changed over time based on age, sex, and education.

    They found that dementia incidence decreased by 28.8 percent between 2002 and 2008 and then increased by 25.2 percent between 2008 and 2016 (nearly 3 percent per year). People with lower educational attainment experienced a slower decline in dementia during 2002-2008 and a more rapid increase after 2008, demonstrating growing disparities. The researchers predicted that if dementia incidence continues to rise at the same pace observed from 2008 to 2016, the number of people living with dementia will roughly double by 2040.

    These findings suggest that the number of people with dementia will be markedly higher in the coming decades. Evidence suggests lifestyle factors influence a person’s dementia risk. Learn how sauna use, exercise, sleep, and dietary components, such as omega-3 fatty acids and sulforaphane exert robust anti-aging effects on the brain, potentially preventing or forestalling dementia.

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  • Enhancing brain health in older adults: Olfactory stimulation via aromatherapy shows promise in cognitive function preservation. neurosciencenews.com
    Brain Alzheimer's Memory Dementia Nose

    The limbic system – a complex system of nerves and networks in the brain – supports many brain functions, including memory, emotion, and learning. The olfactory system is the only sensory system directly linked to this critical brain region. A new study shows that olfactory stimulation via aromatherapy may enhance limbic system function, potentially preserving or improving cognitive function in older adults.

    Researchers assigned 23 older adults (aged 60 to 85) to an olfactory-enriched or control group. Using an aromatherapy diffuser, they exposed the enriched group to seven essential oil scents (rose, orange, eucalyptus, lemon, peppermint, rosemary, and lavender – one per night) for two hours per night for six months. They exposed the control group to a similar routine but with minimal amounts of scent. The participants underwent neuropsychological assessments and functional magnetic resonance imaging (fMRI) scans at the study’s outset and again after six months.

    The assessments revealed that the participants who received olfactory enrichment demonstrated a 226 percent improvement on learning and memory tests. Notably, only six of the 12 participants improved, five stayed the same, and one did worse, calling the data into question. The fMRIs showed that the enriched group also exhibited enhanced function in the left uncinate fasciculus – an area of the brain that plays a crucial role in memory, language, emotion, and memory retrieval.

    These findings suggest that olfactory enrichment administered at night improves cognitive and neural functioning and may provide an effective and low-effort means to improve brain health. This study was very small, so larger trials are needed to confirm the benefits of aromatherapy on cognitive health.

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  • DHA-rich diet protects against memory deficits and loss of smell in Alzheimer's-prone APOE4 mice, reveals new study. link.springer.com
    Brain Alzheimer's Aging Omega-3 Memory Genetics

    A diminished or lost sense of smell is a common feature of the early stages of Alzheimer’s disease and other forms of dementia. But a new study in mice that carry the APOE4 gene variant, the primary genetic risk factor for Alzheimer’s disease, shows that DHA – a type of omega-3 fatty acid found in fish – protects against these losses. APOE4-carrying mice that ate a DHA-rich diet retained their sense of smell and the ability to distinguish between objects based on their scent.

    Researchers fed normal mice and APOE4 carriers a regular diet or one supplemented with DHA. Then, using MRI scans, they assessed the animals' brain structures and studied their behavior related to smell and the recognition of new objects. They also measured biomarkers related to cell death and inflammation.

    They found that the APOE4-carrying mice given a regular diet exhibited memory deficits and difficulty adjusting to new smells and distinguishing between different objects. In addition, their brains showed increased signs of inflammation in the olfactory bulb – the area responsible for the sense of smell. However, APOE4-carrying mice that ate the DHA-rich diet did not exhibit these characteristics.

    These findings suggest that a DHA-rich diet benefits APOE4 carriers. Learn more about the beneficial effects of DHA in our comprehensive omega-3 overview article.

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  • Blocking the body's antiviral immune response holds promise for Alzheimer's disease prevention. medicalxpress.com
    Alzheimer's Aging Immune System Virus

    The immune system plays important, and sometimes surprising, roles in brain health. A new study in mice found that blocking components of the antiviral immune response may make the brain more resilient to the effects of abnormal tau – potentially preventing Alzheimer’s disease and other forms of dementia.

    Tau is a protein found in the brain. Abnormal tau can form aggregates called tau tangles – one of the defining characteristics of Alzheimer’s disease – activating antiviral response pathways and interfering with normal brain function and cognition.

    Researchers studied the effects of exposure to abnormal tau on microglia, the brain’s resident immune cells. They found that when microglia were exposed to abnormal tau, the mitochondria became “leaky,” releasing their DNA into the cellular fluid. The immune system inappropriately interpreted the leaked DNA as a viral attack, triggering an immune response that promoted the release of type-I interferon, a cytokine that drives the antiviral immune response. Interrupting the pathways involved in this response restored normal brain function.

    These findings suggest that suppressing the inappropriate immune response to abnormal tau exposure could provide a means to prevent or treat the tau-associated pathologies common in Alzheimer’s disease and dementia. Learn about other strategies to reduce the risk of Alzheimer’s disease in this episode featuring Dr. Dale Bredesen.

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  • Three or more concussions may worsen brain function later in life. www.sciencedaily.com
    Brain Alzheimer's Aging Dementia Concussion Lactate

    Experiencing multiple concussions increases a person’s risk of poor brain function later in life, a new study shows. People who experienced three or more concussions exhibited cognitive deficits that worsened with each subsequent concussion.

    Researchers collected self-reported concussion histories from more than 5,700 adults between 50 and 70 years old. They administered cognitive tests to gauge changes in the participants' brain function every year for up to four years.

    They found that participants who experienced three mild concussions in their lifetime had difficulty with attention and performing complex tasks later in life. Participants who experienced four mild concussions had difficulty with processing speed and working memory – an aspect of cognitive function that allows a person to remember information for relevant tasks. However, experiencing even one moderate-to-severe concussion impaired the participants' attention and the ability to perform complex tasks and process information.

    These findings underscore the risks associated with even mild brain injury. Some evidence suggests that lactate and ketones may be beneficial in treating brain injury. Learn more in this clip featuring Dr. Dominic D'Agostino.

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  • The effects of obesity on the brain mirror those of Alzheimer's disease. www.sciencedaily.com
    Brain Alzheimer's Obesity Aging

    Excess body weight drives gray matter losses similar to those seen in Alzheimer’s disease, a new study shows. The brains of people who were obese showed marked signs of gray matter atrophy in areas of the brain responsible for attention, problem-solving, and reasoning.

    Using neuroimaging data, researchers compared the grey matter patterns of more than 1,300 older adults. Participants included those with Alzheimer’s disease and those who were cognitively healthy, obese but otherwise healthy, or lean.

    The scientists found that obesity and Alzheimer’s disease had similar effects on the brain. Both conditions were associated with gray matter atrophy in the right temporoparietal cortex (an area involved in attention) and the left prefrontal cortex (an area involved in reason, problem-solving, and comprehension). They also found that obesity-related gray matter atrophy patterns didn’t overlap with amyloid-beta or tau protein distribution in the brains of people with Alzheimer’s disease. Amyloid-beta and tau accumulation are widely considered hallmarks of Alzheimer’s disease.

    Excess body weight drives many metabolic disorders, including type 2 diabetes, hypertension, and dyslipidemia. Recent evidence demonstrates that excess body weight impairs cognitive function. The findings from this study suggest that excess body weight drives gray matter losses similar to those seen in Alzheimer’s disease.

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  • Study shows people with a high omega-3 DHA level in their blood are at 49% lower risk of Alzheimer’s www.eurekalert.org
    Alzheimer's Omega-3

    Higher DHA concentrations cut Alzheimer’s disease risk by half.

    Docosahexaenoic acid (DHA) is an omega-3 fatty acid found in krill oil and the meat and roe of salmon, flying fish, and pollock. When consumed in the diet (or obtained from dietary supplements), DHA preferentially accumulates in the human brain, where it plays essential roles in normal brain function. Findings from a recent study suggest that higher concentrations of DHA in red blood cells protect against Alzheimer’s disease.

    The concentration of omega-3 fatty acids in red blood cells, referred to as the “omega-3 index,” is an indicator of long-term omega-3 exposure, analogous to the HbA1c test for long-term blood glucose concentrations. In general, people who have high blood concentrations – an omega-3 index of about 8 to 12 percent – are far less likely to die from all causes of premature death than those with lower concentrations.

    The investigators drew on data collected in the Framingham Offspring Cohort study, an ongoing study of the effects of lifestyle risk factors on cardiovascular, neurological, and other types of disease outcomes across three generations of participants. Their investigation, which involved nearly 1,500 adults (65 years and older) who did not have dementia, examined whether red blood cell concentrations of DHA influenced the participants' Alzheimer’s disease risk, especially those who carried the APOE4 gene, the primary genetic risk factor for the disease. They categorized the DHA concentrations across five levels and tracked the participants' health for seven years.

    They found that participants whose red blood cell DHA concentrations were in the top fifth were roughly half as likely to develop Alzheimer’s disease during the follow-up period than those in the lowest fifth. This protective effect of DHA translated to nearly five years of life free of Alzheimer’s disease. Higher DHA concentrations conferred more than seven years of protection for participants with the APOE4 gene, suggesting that promoting DHA intake among this susceptible group could have marked effects on their neurological health.

    These findings suggest that higher concentrations of DHA, a type of omega-3 fatty acid, protect against Alzheimer’s disease, especially among carriers of the APOE4 gene. Learn more about the beneficial health effects of omega-3s in this episode featuring Dr. Bill Harris. And for more information about how DHA influences Alzheimer’s disease risk, check out this open-access, peer-reviewed article by Dr. Rhonda Patrick.

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  • Lost memory in menopause explained: Estrogen provides a protective role in mitigating effects of visceral fat on brain structural networks and memory jamanetwork.com
    Brain Alzheimer's Obesity Memory Estrogen Visceral Fat

    Estrogen mitigates the association between visceral fat on cognitive decline.

    Estradiol, a form of estrogen, is the primary female sex hormone. It participates in menstrual cycle regulation and drives the development of female secondary sex characteristics, such as breasts, a wider pelvis, and gynoid fat – fat that forms around the hips, thighs, and breasts. Evidence suggests that estradiol exerts both cardioprotective and neuroprotective effects. Findings from a 2020 study demonstrate that estradiol mitigates the association between visceral fat on cognitive decline.

    Cognitive decline is characterized by altered brain structural networks and accelerated degeneration with aging. Scientists don’t fully understand the biological mechanisms that drive cognitive decline, but evidence indicates that visceral fat – a type of fat that accumulates in the abdominal cavity – may play a role. Visceral fat is metabolically active and is associated with increased markers of inflammation and oxidative stress, and decreased levels of anti-inflammatory proteins, such as adiponectin

    The cross-sectional study involved 974 cognitively healthy females and males (average age, ~50 years). Using magnetic resonance imaging, the investigators measured the participants' gray matter volume, cerebral cortex area, intracranial blood vessels, and visceral fat. They also measured estradiol concentrations in a subset (390) of the females. All the participants completed neuropsychological testing to assess memory performance.

    The investigators found that visceral fat exacerbated the harmful effects of aging on the brain’s structural networks in both females and males. However, estradiol mitigated some of these effects in the females, but not the males. Females between the ages of 35 and 55 years (the period surrounding menopause) who had lower estradiol concentrations were more likely to exhibit greater structural network impairments and worse memory performance.

    These findings suggest that estradiol mitigates some of the harmful effects of visceral fat on the brain’s structural networks and cognitive health. Interestingly, the fasting-mimicking diet preferentially depletes visceral fat. Learn more in this clip featuring Dr. Valter Longo.

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  • Peripheral amyloid-beta produced in the liver in type 2 diabetes may be a crucial link to Alzheimer’s disease www.sciencedaily.com
    Brain Alzheimer's Diabetes Neurodegeneration

    Amyloid-beta produced in peripheral tissues provides a link between diabetes and Alzheimer’s disease risk.

    Type 2 diabetes, a metabolic disorder characterized by glucose intolerance and insulin resistance, poses a significant public health concern, affecting roughly 470 million people worldwide. Having type 2 diabetes greatly increases a person’s risk of developing Alzheimer’s disease, but scientists don’t fully understand the mechanisms that drive the increased risk. Findings from a recent study suggest that amyloid-beta produced in tissues outside the brain provides the link between type 2 diabetes and Alzheimer’s disease.

    Amyloid-beta, a toxic peptide produced in the brain, clumps together and forms plaques with age. Its accumulation is a pathological hallmark of Alzheimer’s disease. However, amyloid-beta is produced in peripheral tissues, as well, including those that are sensitive to glucose or insulin, such as the pancreas, adipose tissues, skeletal muscles, and liver. Scientists don’t fully understand the roles peripheral amyloid-beta plays in human health.

    The investigators conducted a three-part experiment in mice, live mouse tissues, and cell cultures. First, they injected mice with glucose after they had fasted for 16 hours to examine the effects of glucose and insulin on blood amyloid-beta levels. They found that the mice experienced a transient increase in blood levels of glucose, insulin, and amyloid-beta. Then they injected amyloid-beta and glucose into mice that can’t produce the protein and found that amyloid-beta suppressed the animals’ insulin response.

    Next, they applied glucose and insulin to live tissues from the pancreas, adipose tissue, skeletal muscle, liver, and kidneys of mice. They found that glucose stimulated the release of amyloid-beta from the pancreas, whereas insulin stimulated its release from adipose tissue, skeletal muscle, and liver tissue. However, when the scientists added glucose along with amyloid-beta to the pancreatic tissue, insulin release was suppressed.

    Finally, they used antibodies that target the amyloid-beta protein to determine where the protein was produced. They found that amyloid-beta was produced and stored in the beta cells of the pancreas and released into circulation when stimulated with glucose.

    These findings suggest that amyloid-beta protein produced in peripheral tissues modulates insulin secretion. They may further provide a mechanism linking type 2 diabetes to Alzheimer’s disease. The investigators posited that high blood glucose and insulin levels that occur in the setting of diabetes increase peripheral amyloid-beta production, altering the balance between brain and peripheral amyloid-beta levels and suppressing the protein’s efflux from the brain. Furthermore, high insulin levels in the brain may impair normal degradation of brain amyloid-beta, increasing the protein’s levels in the brain and driving its accumulation. Learn more about the role of amyloid-beta in Alzheimer’s disease in this clip featuring Dr. Dale Bredesen.

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  • Loss of Neurons, Not Lack of Sleep, Makes Alzheimer’s Patients Drowsy neurosciencenews.com
    Alzheimer's

    Neuron losses in the brain promote daytime sleepiness in Alzheimer’s disease.

    Scientists have long believed that poor nighttime sleep drives the daytime sleepiness often experienced by people with Alzheimer’s disease. However, findings from a recent study suggest that the loss of wake-promoting neurons in the brain promotes daytime sleepiness in people with Alzheimer’s disease.

    During nighttime sleep, the brain activates the glymphatic system, a self-cleaning process that rids the brain of toxic products, including amyloid-beta and tau tangles. Poor sleep promotes the accumulation of these products, which in turn, promotes poor sleep, creating a vicious cycle that affects brain health. Amyloid-beta accumulation and tau tangle formation are the primary pathological hallmarks of Alzheimer’s disease.

    The investigators recruited 33 people with Alzheimer’s disease, 20 people with progressive supranuclear palsy (a rare neurological disorder that affects balance, movement, vision, speech and swallowing), and 32 healthy people to participate in the study. They assessed the participants' brain activity using electroencephalography and assessed their sleep quality using polysomnography. Upon the participants' deaths, the investigators examined the participants' brains for neuronal changes and the presence of amyloid-beta or tau.

    They found that people with Alzheimer’s disease exhibited an increased desire to sleep and exhibited fewer wake-promoting neurons in their brains, promoting daytime sleepiness. Conversely, people with progressive supranuclear palsy had a decreased desire to sleep and exhibited fewer sleep-promoting neurons, robbing them of the ability to fall asleep and causing sleep deprivation. The dominant toxic protein in the participants' brains was tau.

    These findings suggest that neuronal losses in the brains of people with neurodegenerative disorders contributes to sleep irregularities, and these losses are due to tau accumulation. Learn more about the role of sleep in neurodegenerative disorders in this clip featuring Dr. Matt Walker.

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  • Medium chain triglycerides (MCTs) improved cognition in patients with Alzheimer's disease. www.ncbi.nlm.nih.gov
    Brain Alzheimer's Neurodegeneration

    Medium-chain triglycerides improve cognitive function in Alzheimer’s disease.

    The brain relies heavily on glucose as its primary fuel, burning as much as 130 grams of glucose per day. However, glucose metabolism in the brain is impaired in Alzheimer’s disease, contributing to many of the disease’s symptoms. Findings from a recent study demonstrate that ketones derived from medium chain triglyceride metabolism may provide an alternative fuel source for the brain in the setting of Alzheimer’s disease.

    Ketones are molecules produced by the liver during the breakdown of fatty acids. Ketone production occurs during periods of low food intake (such as during fasting), carbohydrate-restrictive diets, starvation, or prolonged intense exercise. Humans produce three types of ketones: acetoacetate, beta-hydroxybutyrate, and acetone. Ketones are readily used as energy by a diverse array of cell types, including neurons, and some evidence suggests that ketones improve cognitive function.

    Medium-chain triglycerides (MCTs) are a class of saturated fats. They are composed of medium-length fatty acid chains (six to 12 carbons long) bound by a glycerol backbone. Medium-chain triglycerides occur naturally in coconut oil, palm oil, and butter, but they can also be synthesized in a laboratory or food processing setting and provided as dietary supplements.

    The randomized, placebo-controlled trial involved 20 adults between the ages of 53 and 84 years who had been diagnosed with Alzheimer’s disease. The investigators used a crossover design, which allows all participants to receive the same treatment, at different times. In this trial, half of the participants received an average of two tablespoons of MCTs daily for three months, while the other half received a comparable amount of olive oil for the same duration. Then the participants switched to the opposite treatment. Participants underwent cognitive testing before, during, and after the intervention. After completing both forms of the intervention, all the participants received MCTs for six months. The investigators collected the participants' demographic and health data, which included measures of blood lipids, fasting insulin, body mass index, and body fat composition.

    They found that 80 percent of the participants demonstrated improved or stable cognitive function while taking the MCTs. The greatest improvements were seen among participants who received MCTs last (providing them nine months of uninterrupted treatment) and among those who were older than 73 years.

    These findings suggest that long-term MCT intake stabilizes cognitive function in adults with Alzheimer’s disease, especially in mild to moderate disease. This was a small study, however, so larger studies are needed to confirm these findings.

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  • Brain’s own immune cells "infect" healthy neurons with Alzheimer-linked beta-amyloid protein. www.nature.com
    Alzheimer's Immune System

    Alzheimer’s disease is a common neurodegenerative disorder affecting an estimated 24 million older adults worldwide. Researchers believe the disease is caused by toxic levels of beta-amyloid protein aggregates in the brain that impair neuronal function and trigger cognitive decline. While this process is partly under the influence of genes, studies also indicate links between Alzheimer’s and external factors such as head injury. Findings from a new study shed new light on this link, suggesting that events such as head trauma and stroke accelerate Alzheimer’s disease by activating one of the brain’s major immune cells and triggering an infection-like spread of amyloid-beta tangles to previously unaffected tissues.

    The researchers conducted their experiments in mice genetically engineered to carry five mutations associated with Alzheimer’s disease. While these mutations lead to brain beta-amyloid aggregations and cognitive impairments at an early age, the team uncovered that even genetically healthy brain tissue could accumulate these aggregations if implanted into the brains of these mutant mice.

    To better understand this infection-like phenomenon, the researchers examined whether the mutant brain cells of the host might import beta-amyloid particles by migrating into the transplanted tissue or making connections with its neurons. Tracking them under a microscope offered no support for this hypothesis. Instead, the team uncovered a mass migration into the implanted tissue of microglia, the main immune cells of the nervous system, specialized for scouting brain tissue for signs of injury or pathogen invasion and clearing out cellular debris.

    One possible reason for this migration is that microglia are drawn to wounds. Indeed, the microglia were particularly concentrated around the edges of the transplant and exhibited similar migrations to tiny brain lesions that the researchers generated using lasers. However, in moving from the genetically diseased to healthy tissue, the microglia dumped large numbers of beta-amyloid particles previously picked up from the degenerating host brain tissue.

    The results offer an updated picture of Alzheimer’s disease progression where the brain’s own immune cells inadvertently drive the spread of pathogenic beta-amyloid aggregations – an effect that might be aggravated by brain injury events and inflammation. While scientists are uncertain why contaminated microglia engage in this “dumping” practice, targeting the cells' activity as a way of interfering with the neurodegenerative process provides promising research opportunities.

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  • Hypertension in mid-life reduces brain volume and increases risk of dementia. neurosciencenews.com
    Alzheimer's Dementia Blood Pressure Stroke

    Many people develop hypertension (high blood pressure) with age, putting them at risk of cardiovascular disease, chronic kidney disease, retinal damage, and stroke. Hypertension is also a risk factor for Alzheimer’s disease and dementia, due to damage caused by years of vessel injury, microbleeds, and lesions. Authors of a recent study report that hypertension diagnosed in early or midlife, but not late life, is a predictor of dementia.

    Because hypertension damages the delicate small blood vessels of the heart, kidneys, eyes, brain, and other organs, it is a risk factor for a wide range of chronic diseases. Previous research has shown that hypertension, by restricting blood flow, reduces brain volume in key areas associated with dementia, such as the prefrontal cortex and hippocampus. As the number of young adults with hypertension increases to an estimated 1.6 billion globally by 2025, research on the risks of hypertension in earlier life are needed.

    The authors collected data from more than 135,000 participants with hypertension and 135,000 matched control participants without hypertension from the United Kingdom Biobank, a long-term study of United Kingdom citizens. The researchers categorized participants into four categories: younger than 35 years; 35 to 44 years; 45 to 54 years; and 55 to 64 years. They used magnetic resonance imaging data to measure brain volume, and hospital records, death records, and self-reports to assess dementia status. Participants in the study provided data at a baseline appointment between 2006 and 2010 and at a follow-up appointment between 2014 and 2021.

    Participants diagnosed with hypertension at any age had smaller brain volume than their matched control participant without hypertension. Participants diagnosed earlier in life had the greatest reductions, with participants diagnosed between ages 35 and 44 exhibiting a 0.8 percent loss in volume and participants before age 35 exhibiting a 1.2 percent loss. Specifically, hypertension was associated with loss of peripheral cortical gray matter, brain tissue necessary for higher brain functions such as learning, memory, and attention. Participants diagnosed with hypertension between ages 35 and 44 were at a 61 percent higher risk of dementia than the matched control participants without hypertension.

    The authors concluded that hypertension diagnosed in early mid life, but not late life, is associated with decreased brain volume and increased risk of dementia. Lifestyle strategies that reduce blood pressure, such as exercise, sauna use, dietary modification, and stress management, may reduce dementia risk.

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  • Omega-3 fatty acids slow memory loss in people with Alzheimer's disease. apple.news
    Nutrition Alzheimer's Omega-3 Neurodegeneration

    Omega-3 fatty acids are essential for human health. They participate in pathways involved in the biosynthesis of hormones that regulate blood clotting, contraction and relaxation of artery walls, and inflammation. They have been shown to help prevent heart disease and stroke; may help control lupus, eczema, and rheumatoid arthritis; and may play protective roles in cancer and other conditions. Findings from a new study suggest that omega-3 fatty acids slow cognitive decline in Alzheimer’s disease.

    Alzheimer’s disease is a neurodegenerative disorder characterized by progressive memory loss and cognitive decline. The primary risk factor for Alzheimer’s disease is aging, with risk roughly doubling every five years after the age of 65 years. Nutritional status also plays key roles in Alzheimer’s disease risk and pathology. The intervention study involved 33 people who had been diagnosed with Alzheimer’s disease. Approximately half of the participants took a supplement providing 2.3 grams of omega-3 fatty acids daily for six months; the other half took a placebo. All participants took the Mini Mental State Examination (MMSE), a widely accepted measure of memory and cognitive function, before and after the intervention. The study investigators collected cerebrospinal fluid samples before and after the intervention to measure several biomarkers associated with neurodegenerative diseases and inflammation, including amyloid beta proteins, tau, interleukin 6, chitinase-3-like protein 1 (YKL-40), and neurofilament light (NfL). YKL-40 is associated with neuroinflammation, and NfL is associated with damage to the axons of nerves in brain white matter.

    The MMSE scores of the participants who took the omega-3 fatty acid supplements remained stable over the six-month intervention, decreasing by only 0.06 points, but the scores of those who took the placebo decreased by two points. The two groups' biomarkers were similar at the beginning of the intervention, but YKL-40 and NfL increased slightly in the group that received the omega-3 fatty acid supplement, indicating a possible increase in neurodegeneration and inflammatory responses. However, the increase in the two biomarkers did not correlate with the participants' MMSE scores.

    These findings suggest that omega-3 fatty acids help maintain memory and cognitive function in older adults with Alzheimer’s disease. This was a very small study, however, and further research is needed to confirm any protective effects of omega-3 fatty acid intake in Alzheimer’s disease.

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  • Folate reduces risk for Alzheimer’s disease. www.frontiersin.org
    Brain Alzheimer's Micronutrients Folate Neurodegeneration

    Alzheimer’s disease, the most common type of neurodegenerative disease in older adults, causes a progressive deterioration of cognitive function. Recent research indicates that folate (vitamin B9) deficiency may play a role in Alzheimer’s pathology along with other micronutrients, such as vitamin A. A recent systematic review and meta-analysis reports that folate deficiency increases the risk for Alzheimer’s disease.

    Folate is an essential nutrient used by the body to create new DNA and RNA and to metabolize amino acids, all of which are necessary for cell division. Good sources of folate include legumes, such as peanuts and chickpeas, and green vegetables such as spinach and asparagus. Previous research has shown that folate supplementation improves cognitive function in older adults through mechanisms that are not well-understood, but likely involve reduced inflammation. Because dose, population characteristics, and testing methods often vary among clinical trials, coming to a consensus about the efficacy of an investigational treatment presents challenges; however, review articles can be a valuable way to combine and report existing data in a new and helpful way. This study is a systematic review and meta-analysis, meaning that the authors searched existing literature for studies related to folate and Alzherimer’s disease, collected studies based on a set of criteria meant to select for high-quality design, and then combined the data and reanalyzed it.

    The authors selected 59 studies that met their criteria for high-quality design. In a sample of more than 2,000 participants from a collection of case-control studies, participants with folate deficiency (less than 13.5 nanomoles per liter) were more than twice as likely to develop Alzheimer’s disease compared to participants with normal folate status (greater than 13.5 nanomoles per liter). Likewise, data from a collection of five cohort studies revealed that participants with folate deficiency were 88 percent more likely to develop Alzheimer’s disease compared to individuals with sufficient folate status. Finally, in a sample of 11 cohort studies, participants who consumed less than the recommended dietary allowance (400 micrograms) were 70 percent more likely to develop Alzheimer’s disease than those who consumed 400 micrograms of folate per day or more.

    This review of the evidence supports a relationship between folate intake and serum folate concentration in reducing risk for developing Alzheimer’s disease. Future studies should utilize an interventional design to investigate the mechanisms of folate in Alzheimer’s pathology.

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  • Vitamin D deficiency exacerbates inflammation and Alzheimer's pathology in mice. pubmed.ncbi.nlm.nih.gov
    Vitamin D Alzheimer's

    Currently selected for this coming member’s digest by team member Melisa B.

    Adequate exercise is one of the most effective lifestyle interventions to improve aging, but many people, especially older adults, can find it difficult to exercise. In a study published this month, researchers tested the effects of resveratrol as an adjuvant therapy to exercise for older adults with physical limitations.

    The word “adjuvant” has roots in Latin that mean “helping toward.” Adjuvant therapies are add-ons that may improve the effectiveness of other interventions. Resveratrol is known to activate mitochondria through a protein called PGC-1α, the master regulator of mitochondrial biogenesis. Therefore, resveratrol may boost the benefits of exercise by enhancing mitochondrial adaptation in skeletal muscle.

    The purpose of this randomized controlled pilot study was to determine the safety and feasibility of chronic exercise combined with resveratrol supplementation. The investigators split a group of 60 adults (average age, 71 years) with physical limitations into three groups. All three groups completed supervised walking and whole-body resistance training twice weekly for 12 weeks. One group took 500 milligrams of resveratrol daily, another took 1,000 milligrams of resveratrol daily, and the third group took a placebo. The participants completed a battery of physical function tests and gave blood so the researchers could measure markers of cardiovascular risk.

    On average, participants completed 82 percent of their exercise sessions and took 85 percent of their resveratrol doses, indicating that the intervention was acceptable for most participants. The rate of adverse events was similar between groups with an average of nine events, indicating that the intervention was safe. Pilot studies are not designed to evaluate the effect of the study intervention on health; however, the authors reported some promising early results. Participants in the 1,000 milligram group exhibited a clinically-significant increase of 449 meters in their 6-minute walk test and increased levels of citrate synthase, a common marker of mitochondrial volume.

    The authors are planning a large-scale clinical trial to build on these preliminary results.

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  • Nanoparticles in air pollution accumulate in the brains of young adults: A common denominator in neurodegenerative disease? www.sciencedaily.com
    Alzheimer's Parkinson's Development Pollution

    Alzheimer’s disease (AD) and Parkinson’s disease (PD) are the two most common neurodegenerative conditions in older adults, affecting a combined 36 million people worldwide. Evidence suggests that exposure to air pollution increases the risk of developing these diseases. Findings from a recent study demonstrate that particulate matter in air pollution accumulates in the brains of young adults and may serve as a common denominator in the pathophysiology of AD and PD.

    Particulate matter in air pollution is a mixture of solid particles and liquid droplets. It is present in fine inhalable particles, with diameters that are generally 2.5 micrograms or less. Ultrafine particles less than 1 microgram in diameter, referred to as nanoparticles, are often enriched in highly reactive metals such as iron, aluminum, titanium, and others. They may serve as catalysts for reactive oxygen species formation and promote protein misfolding and aggregation. Nanoparticles in air pollution are not regulated and carry many health risks. They are also present in food additives and food packaging materials.

    The authors of the study documented biomarkers of AD and PD present in brainstem samples taken during the autopsies of 186 healthy children and young adults (age range, 11 months to 27 years) living in the metro area of Mexico City, a region known for its high levels of air pollution. They also conducted magnetic remanence studies to quantify the presence of metal-rich nanoparticles in the brainstem samples. Finally, using high resolution scanning and transmission electron microscopy and energy-dispersive X ray analysis, they identified the composition, location, size, and shape of nanoparticles in the substantia nigra region of a randomly chosen single sample taken from the larger group. Damage to the substantia nigra is a hallmark of PD.

    They found that all of the brainstem samples contained iron-, aluminum-, and titanium-rich nanoparticles. The quantity of nanoparticles varied among the brain samples, likely due to the level and duration of exposure. The authors posited that these nanoparticles could have been acquired via both oral and respiratory routes from food sources and airborne exposures, respectively. Damage to the mitochondria, endoplasmic reticulum, and neuromelanin in the single brainstem sample correlated with the presence of iron-, aluminum-, and titanium-rich nanoparticles.

    These findings suggest that exposure to nanoparticles is pervasive, with evidence confirmed as early as 11 months of age. Such exposures may put people living in urban areas where high levels of air pollutants are present at greater risk for developing AD and PD.

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  • New blood test diagnoses Alzheimer's disease decades before symptoms manifest. www.eurekalert.org
    Alzheimer's

    Alzheimer’s disease is a neurodegenerative disorder characterized by progressive memory loss, cognitive decline, and behavioral changes. Roughly 50 million people have Alzheimer’s disease worldwide. Researchers have developed a blood test that measures phospho-tau217 (p-tau217), a type of tau protein, and may be useful in diagnosing Alzheimer’s disease as early as 20 years before symptoms manifest.

    Tau is a protein that clumps together and forms tangles inside neurons in the brains of people with Alzheimer’s disease. When tau tangles form, the system for transporting mitochondria, lipids, and cellular metabolites is disrupted. As a result, cellular energy is reduced, and new synapse formation is halted, resulting in impaired memory, a hallmark of Alzheimer’s disease. Typically, the presence of tau tangles is determined during autopsy, but it can be observed via PET imaging studies in living persons.

    The study involved more than 1,400 people from three cross-sectional cohorts. Some of the participants were cognitively impaired, while others were not. The three cohorts provided data from clinical, neuropathological, imaging, cerebrospinal fluid, blood-based biomarker, and genetic assessments.

    The authors of the study found that the p-tau217 blood test distinguished the presence of Alzheimer’s disease from other neurodegenerative diseases better than currently used biomarkers and equally as well as imaging studies. The test identified early signs of Alzheimer’s disease in people who were genetically predisposed to the condition as much as 20 years before the onset of symptoms. These findings suggest that a simple blood test could accurately diagnose Alzheimer’s disease early in its pathology, potentially providing strategies to delay or prevent the disease.

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  • Carriers of a common BDNF genetic variant demonstrate more rapid decline from Alzheimer's disease. www.sciencedaily.com
    Brain Alzheimer's Genetics BDNF Neurodegeneration

    BDNF plays critical roles in many aspects of cognitive function, including learning and memory formation. A single-nucleotide polymorphism (SNP) in the gene that encodes BDNF causes a substitution of the amino acid valine (Val) by methionine (Met) in a specific region of the DNA where the gene is located. Evidence suggests that carrying the Met allele (Met/Met or Val/Met genotype) is associated with lower BDNF expression.. A 2017 study found that amyloid-beta burden impaired BDNF-related learning and memory.

    Amyloid-beta is a toxic 42-amino acid peptide that aggregates and forms plaques in the brain with age. Amyloid-beta is associated with Alzheimer’s disease, a progressive neurodegenerative disease that can occur in middle or old age and is the most common cause of dementia.

    The study involved more than 1,000 adults (approximately 55 years at the beginning of the study) who were enrolled in a larger study of Alzheimer’s disease. Nearly 65 percent of the participants were at high risk for developing Alzheimer’s disease, having at least one parent diagnosed with the condition. Each of the participants underwent cognitive assessment and BDNF genotyping five times over a period of four to 11 years. In addition, a small cohort of participants underwent imaging studies to assess amyloid-beta burden.

    The genotyping revealed that approximately one-third of the participants were carriers of the Met-66 allele. Compared to Val/Val carriers, Met-66 carriers showed steeper declines in cognitive function. In addition, Met-66 carriers with greater amyloid-beta burden showed an even greater cognitive decline, likely due to lower BDNF expression. These findings suggest that a SNP in the gene for BDNF influences cognitive health and could serve as a therapeutic target against Alzheimer’s disease.

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  • Preclinical evidence suggests BDNF may be a potent interventional tool in Alzheimer's and brain aging by directly improving learning and memory www.sciencedaily.com
    Exercise Brain Alzheimer's Aging Memory BDNF

    From the article:

    For these experiments, the researchers injected the BDNF gene or protein in a series of cell culture and animal models, including transgenic mouse models of Alzheimer’s disease; aged rats; rats with induced damage to the entorhinal cortex; aged rhesus monkeys, and monkeys with entorhinal cortex damage.

    In each case, when compared with control groups not treated with BDNF, the treated animals demonstrated significant improvement in the performance of a variety of learning and memory tests. Notably, the brains of the treated animals also exhibited restored BDNF gene expression, enhanced cell size, improved cell signaling, and activation of function in neurons that would otherwise have degenerated, compared to untreated animals. These benefits extended to the degenerating hippocampus where short-term memory is processed, one of the first regions of the brain to suffer damage in Alzheimer’s disease.

    […]

    “In this series of studies, we have shown that BDNF targets the cortical cells themselves, preventing their death, stimulating their function, and improving learning and memory. Thus, BDNF treatment can potentially provide long-lasting protection by slowing, or even stopping disease progression in the cortical regions that receive treatment.”

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  • Beta-hydroxybutyrate, a ketone, increases brain-derived neurotrophic factor expression: relevance for neurodegenerative disease www.sciencedaily.com
    Exercise Brain Alzheimer's Diet Ketosis BDNF HDAC Inhibitor

    β-hydroxybutyrate production consequent to exercise induces within the muscle the activities of a key promoter involved in the production of brain-derived neurotrophic factor.

    From the article:

    Studies have shown that BDNF levels in the brains of people with Alzheimer’s or Huntington’s disease are, on average, half that of people without either brain-damaging disease.

    Among the key findings of the current study was that a ketone, a chemical naturally produced in the liver called beta-hydroxybutyrate (DBHB), triggers biological reactions that activate the BDNF gene to produce more of its protein. DBHB has long been known to build up in the body and brain with exercise. Ketones are “by-product” chemicals made when animals break down fat as an alternative energy source after having drained more readily available sugar stores during exercise.

    Specifically, Chao says, the researchers found that DBHB prevents other proteins in the brain known as histone deacetylase complexes, or HDACs, from suppressing BDNF production by altering the environment of the BDNF gene.

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  • Greater BDNF expression in brain tied to up to 50% slower decline in memory in older people (for those in top decile of expression) www.sciencedaily.com
    Brain Alzheimer's Memory Dementia BDNF

    A study of BDNF gene expression in post-mortem brain tissue found that BDNF may provide a buffer against dementia, particularly when higher expression is found in the context of the classical Alzheimer’s brain pathology of amyloid-beta plaques and tau tangles.

    From the article:

    For the study, 535 people with an average age of 81 were followed until death, for an average of six years. They took yearly tests of their thinking and memory skills, and after death, a neurologist reviewed their records and determined whether they had dementia, some memory and thinking problems called mild cognitive impairment or no thinking and memory problems. Autopsies were conducted on their brains after death, and the amount of protein from BDNF gene expression in the brain was then measured.

    […]

    The rate of cognitive decline was about 50 percent slower for those in the highest 10 percent of protein from BDNF gene expression compared to the lowest 10 percent. The effect of plaques and tangles in the brain on cognitive decline was reduced for people with high levels of BDNF. In the people with the highest amount of Alzheimer’s disease hallmarks in their brains, cognitive decline was about 40 percent slower for people with the highest amount of protein from BDNF gene expression compared to those with the lowest amount.

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