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Neurodegeneration

Polyphenol-rich diets and neurodegeneration (glycemic control) featured article

Our brains shrink as we grow older, but that doesn't mean you can wait until old age to worry about it—neurodegeneration starts 15–20 years before the onset of symptoms of mild cognitive impairment, dementia, or Alzheimer's disease.

Certain brain structures, like the hippocampus, are particularly vulnerable, accumulating neurofibrillary tangles, undergoing a reduction in synapses, and losing neurons.

The good news is that we can intervene in the process, and one of the most important ways to do this is to keep blood glucose levels in check.

Glucose levels that fall within the high-normal range are associated with an atrophying of the hippocampus. It gets even worse for people with metabolic dysfunction or diabetes, who have higher levels of brain atrophy—hence why Alzheimer's disease is sometimes referred to as "type 3 diabetes." Glucose control is a modifiable risk factor for cognitive decline.

How can one bolster metabolic health in an attempt to stave off brain...

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Episodes

ketogenic diet

Neurological disorders and migraines | Dominic D'Agostino

Posted on May 21st 2022 (about 3 years)

In this clip, Dr. Dominic D'Agostino describes how nutritional ketosis may support the treatment of neurodegenerative and other brain disorders.

parkinson's

Importance of intensity of exercise and dopamine in treating Parkinson's | Giselle Petzinger

Posted on October 28th 2020 (over 4 years)

In this clip, Dr. Giselle Petzinger discusses how intense exercise can impact motor scores in people with Parkinson's disease.

parkinson's

Exercise improves sensitivity to dopamine | Giselle Petzinger

Posted on October 28th 2020 (over 4 years)

In this clip, Dr. Giselle Petzinger explains that strenuous exercise affects dopamine sensitivity in the brains of people with Parkinson's disease.

Topic Pages

  • Creatine

    Mechanistically, creatine buffers neuronal ATP via the phosphocreatine shuttle, mitigating neurodegeneration-induced mitochondrial energy failure.

  • Nicotinamide mononucleotide

    Nicotinamide mononucleotide replenishes NAD+, activating sirtuins and PARP-mediated repair pathways, mitigating mitochondrial dysfunction implicated in neurodegeneration.

  • Senescence

    Senescent glial cells secrete SASP cytokines, ROS and proteases, triggering neuroinflammation, synaptic dysfunction and progressive neurodegeneration.

News & Publications

  • Sleep enhances the brain's waste removal through synchronized fluctuations in norepinephrine and blood volume, a process disrupted by the common sleep aid, zolpidem. https://www.cell.com/cell/abstract/S0092-8674\(24\)01343-6
    Brain Sleep Norepinephrine Neurodegeneration

    The brain doesn’t just rest during sleep—it actively clears out waste that can damage brain cells. This crucial process, known as glymphatic clearance, relies on the movement of cerebrospinal fluid to wash away harmful proteins linked to neurodegenerative diseases. A recent study found that synchronized fluctuations in norepinephrine, blood volume, and cerebrospinal fluid are key drivers of glymphatic clearance during deep sleep, but some popular sleeping pills disrupt this process.

    The researchers tracked blood and cerebrospinal fluid dynamics while mice slept naturally. Then, they examined how zolpidem, commonly known as Ambien, affected these dynamics during sleep.

    They found that norepinephrine fluctuations triggered by the brain’s locus coeruleus drove rhythmic changes in blood vessel size. This facilitated the movement of cerebrospinal fluid into the brain and the removal of waste products. However, zolpidem disrupted norepinephrine activity, reducing cerebrospinal fluid flow and hindering this waste removal process.

    These findings suggest that the brain’s waste removal system relies on a delicate balance of norepinephrine and blood vessel activity. Sleep aids like zolpidem disrupt this process, potentially contributing to neurodegenerative diseases like Alzheimer’s. Learn more about the effects of sleep aids like Ambien in this episode featuring Dr. Matthew Walker.

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  • Mechanical stresses and myokines produced by muscles during exercise synergistically promote nerve growth and connectivity. onlinelibrary.wiley.com
    Exercise Muscle Neurodegeneration

    Muscle contraction, the hallmark of exercise, releases signaling molecules called myokines that influence cell function throughout the body. However, the mechanical forces it generates may also play a role. A recent lab study found that biochemical and mechanical signals from contracting muscle work synergistically to promote nerve growth and maturation.

    Researchers grew muscle cells on a specialized gel that mimicked the movements of contracting muscles. Then, by adding tiny magnetic particles, they stretched the cells to simulate exercise. They assessed how these forces and the myokines released by the muscle cells influenced the growth of nerve cells.

    They found that nerve cells grew and migrated more readily when exposed to myokines from contracting muscle cells, with more robust effects at higher levels of muscle activity. Stretching the nerve cells mechanically produced similar growth, but further analysis demonstrated that chemical signals were more effective in activating genes related to nerve growth and forming connections.

    These findings suggest that exercise influences nerve health through biochemical and mechanical pathways, providing new insights into how muscle activity supports the nervous system. Myokines also exert anti-cancer effects. Learn more in this episode featuring Dr. Rhonda Patrick.

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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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  • 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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  • Rebalancing gut microbiome with butyrate lengthens survival in mouse model of ALS by repairing intestinal permeability www.sciencedaily.com
    Brain Aging Microbiome Neurodegeneration Butyrate Intestinal Permeability

    From the article:

    In a mouse model of ALS, the compound butyrate helped correct a gut microbiome imbalance and reduced gut leakiness – both symptoms of ALS. The treated mice lived also longer compared to mice that weren’t given butyrate.

    […]

    When the researchers fed the ALS-prone mice butyrate in their water, starting when the mice were 35 to 42 days old, the mice showed a restored gut microbiome profile and improved gut integrity. Butyrate-treated mice also showed improved neuromuscular function and delayed onset of ALS symptoms. Treated mice showed symptoms at 150 days old compared to control mice at about 110 days. Treated mice also lived an average 38 days longer than mice not given butyrate.

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  • Particulate matter in wildfires harms the brain. www.eurekalert.org
    Pollution Neurodegeneration

    Global climate change is driving an increase in wildfire activity characterized by larger fires and longer fire seasons. Wildfire smoke, which can spread over immense geographical areas, often contains a variety of pollutants and exerts a wide range of adverse effects on human health. Evidence from a new rodent study suggests that particulate matter in wildfires drives neuroinflammation, increasing the risk for neurodegenerative diseases.

    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 (PM2.5) 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. Exposure to particulate matter in air pollution promotes oxidative stress, increases the risk of developing many chronic diseases, and accelerates aging.

    The investigators studied the effects of wildfire smoke on mice that were housed in a mobile lab located roughly 186 miles (300 kilometers) away from naturally occurring wildfires in the western United States. They exposed the mice to the smoke for four hours every day for 20 days and assessed the animals' immune and inflammatory responses.

    They found that the animals were exposed to high levels of PM2.5. This exposure switched on the activity of brain microglia (immune cells); promoted the infiltration of pro-inflammatory immune cells and molecules into the brain tissues; and increased accumulation of amyloid-beta 42, a toxic protein associated with Alzheimer’s disease and neurodegeneration. Particulate matter exposure also decreased the production of compounds that protect the brain against aging, such as nicotinamide adenine dinucleotide (commonly known as NAD+) and taurine.

    These findings suggest that exposure to PM2.5 in wildfire smoke elicits harmful effects on the brain via activation of immune and inflammatory responses. The investigators noted that the mobile lab used in this study was located a considerable distance from the smoke sources, likely diluting the animals' exposure and reflecting PM2.5 exposures far lower than those experienced by humans living closer to the fires.

    Robust evidence demonstrates that HEPA filter air purifiers reduce indoor PM2.5 concentrations and improve health outcomes, and many government agencies and public health authorities recommend the use of indoor HEPA filters to reduce wildfire smoke exposure and its negative health effects. In addition, well-fitting N95 masks and equivalent respirators can reduce PM2.5 exposure. Interestingly, dietary consumption of omega-3 fatty acids may help protect the brain from damage associated with PM2.5 exposure. Learn more about the health effects of omega-3 fatty acids in this episode featuring Dr. Bill Harris.

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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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  • Whole-body hyperthermia activates muscle hormone irisin and increases neuroprotective factors. www.sciencedirect.com
    Exercise Brain Muscle Sauna BDNF Neurodegeneration

    Exposure to high heat while sauna bathing causes mild hyperthermia – an increase in the body’s core temperature – that induces a thermoregulatory response to restore homeostasis and condition the body for future heat stressors. These adaptations to high temperatures involve increased production of brain derived neurotrophic factor (BDNF), a promoter of neuroplasticity, and irisin, a biomarker of exercise. Findings of a new report demonstrate that whole-body hyperthermia increases BDNF and irisin in healthy young adults.

    Whole-body hyperthermia is a therapeutic strategy used to treat various diseases, including cancer and depression. Previous research has shown that use of a hyperthermia chamber increases BDNF to a greater extent than light intensity exercise. Some research has suggested that BDNF production is stimulated by irisin, a hormone secreted from muscle in response to exercise. Irisin may mediate some of the beneficial effects of exercise and sauna use in humans, but additional research is needed.

    The authors recruited 20 male participants (average age, 22 years) and assessed their baseline heat tolerance using a hyperthermia protocol. Participants reclined in a hyperthermia chamber while the researchers increased the temperature of the chamber by 50 degrees F every ten minutes until the participant reached their personal heat threshold. Next, participants completed ten hyperthermia sessions tailored to their baseline conditioning, during which the hyperthermia chamber was set to a temperature of 150 to 175 degrees F. Following a three-week wash-out period, they completed ten sham treatments over two weeks, during which the hyperthermia chamber was set to a temperature of 75 to 77 degrees F.

    Participants had an average core body temperature of 102 degrees F at the end of each whole-body hyperthermia treatment. Following ten whole-body hyperthermia treatments, participants had a significant increase in circulating irisin levels (6.3 micrograms per milliliter) compared to their baseline levels (5.0 micrograms per milliliter) and compared to their irisin levels following the sham treatment (5.4 micrograms per milliliter). Whole-body hyperthermia treatment also significantly increased BDNF levels (28.3 picograms per liter) compared to baseline (25.9 picograms per liter).

    In healthy young adults, ten whole-body hyperthermia significantly increased irisin and BDNF levels. The authors noted that future studies should explore the effects of whole-body hyperthermia on adipose tissue, which also produces irisin.

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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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  • COVID-19 may increase a person's risk for neurodegenerative disease. www.sciencedirect.com
    COVID-19 Neurodegeneration

    COVID-19 is an acute illness caused by infection with the SARS-CoV-2 virus. Although most people recover from COVID-19 within a few weeks of presenting with symptoms, some experience long-term complications that affect multiple organs, including the heart, lung, kidney, skin, and brain. Findings from a recent study suggest that SARS-CoV-2 infection may promote neurodegenerative disease.

    Neurodegenerative diseases are chronic disorders of the central nervous system that are characterized by chronic progressive loss of neuronal structure and function. They often emerge in mid-to-late adult life and are increasingly common, affecting roughly 37 million people worldwide – a number expected to increase as human lifespan increases. Although scientists don’t fully understand the underlying causes of most neurodegenerative diseases, protein aggregation in the brain is a widely accepted contributing factor. Previous research has shown that the SARS-CoV-2 spike protein binds to heparin (a protein involved in blood clotting) and heparin binding proteins, accelerating the aggregation of proteins involved in neurodegeneration.

    Since many of the biological functions of a protein depend upon its affinity to bind with other proteins, the authors of the study used a web-based algorithm called HDOCK to gauge the binding affinity between the receptor binding domain of the SARS-CoV-2 spike protein between heparin and several aggregation-prone heparin-binding proteins implicated in neurodegenerative diseases, including amyloid-beta, alpha-synuclein, tau, and TAR DNA binding protein.

    They found that SARS-CoV-2 spike protein exhibited differing binding affinities for the various proteins. Heparin showed the highest affinity, with the others exhibiting affinity in decreasing order: prion, amyloid-beta, tau, TAR DNA binding protein, and alpha-synuclein.

    These findings suggest that the heparin-binding site on the spike protein facilitates the subsequent binding to amyloid proteins, potentially leading to neurodegeneration in the brain. Learn more about risk factors that drive Alzheimer’s disease, a type of neurodegenerative disease, in this episode featuring Dr. Dale Bredesen.

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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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  • Restoration of BDNF-mediated signaling as a potential therapeutic strategy against Huntington's disease. www.sciencedaily.com
    Brain BDNF Neurodegeneration

    Huntington’s disease is a progressive neurodegenerative disorder characterized by uncontrolled movements, speech problems, personality changes, and dementia. The disease is caused by a single genetic mutation, called a CAG repeat, that drives abnormal protein folding and aggregation of the huntingtin protein and subsequent death of striatal neurons. Findings from a 2010 study demonstrate that modulating pathways involved in BDNF-mediated signaling shows promise as a therapeutic against Huntington’s disease.

    Evidence suggests that normal huntingtin promotes the expression of BDNF, but mutated huntingtin impairs it. Striatal neurons need BDNF for their normal function and survival. A critical component in BDNF’s actions on striatal cells is a receptor called TrkB, to which BDNF binds. Levels of TrkB are diminished in Huntington’s disease.

    The authors of the in vitro cell study investigated the effects of BDNF administration on mutant huntingtin. They found that altered cell-signaling in the Ras/MAPK/ERK1/2 pathway in cells expressing mutant huntingtin drove the loss of TrkB receptors, increased striatal cells' sensitivity to oxidative damage, and promoted cell death. These findings suggest that identifying ways to modulate the Ras/MAPK/ERK1/2 pathway and restore BDNF-related signaling shows promise as a therapeutic strategy against Huntington’s disease.

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