Compound found in coffee may improve muscle health and function during aging

 

• Sarcopenia, which is the progressive loss of muscle mass and strength, affects many adults when they get older.
• The loss of muscle mass can contribute to mobility problems, frailty, and subsequent reduction in independence for many older people.
• Researchers, including from Nestle Research, found that a compound found in coffee and fenugreek, but also made in the microbiome in the gut, improves energy metabolism in muscle fibers in humans, mice, and worms.

Sarcopenia describes the loss of skeletal muscle that occurs naturally as we age.

Approximately 10%-16% of people over the age of 65 are thought to be affected worldwide, and prevalence is higher in people with other conditions, for example, cancer and diabetes.

It is a natural part of aging, and the average adult loses about 250g of muscle each year between the ages of 30 and 60, and this accelerates after the age of 70.

This can lead to mobility problems, falls and frailty that often leads to a loss of independence in older people. As such, it represents a significant disease burden in an aging population.

A recent study looking at worms, male mice and tissue samples taken from male participants affected by sarcopenia, investigated the molecular mechanisms underpinning this condition.

They found that a compound found in coffee and fenugreek, but also made in the microbiome in the gut, can improve muscle function in aging humans, mice, and worms.

The results were published in a letter to Nature Metabolism.

Can sarcopenia be stopped?

Dr. Kubanych Takyrbashev the Health and Wellness Advisor at NAO, who has previously worked as a doctor specializing in critical care of older adults, who was not involved in the study, explained to Medical News Today how sarcopenia affects aging humans:

“One of the most concerning implications of sarcopenia is the increased risk of falls and fractures. Declining muscle mass and strength contribute to decreased mobility and agility, making individuals more susceptible to accidents. Additionally, sarcopenia often leads to functional decline and disability, impairing activities of daily living and diminishing independence. Many individuals with sarcopenia require assistance for routine tasks, which can significantly impact their quality of life.”

Past research has indicated that people who engage in physical exercise are less likely to develop sarcopeniaTrusted Source. Poor nutrition including not eating enough proteinTrusted Source is also associated with sarcopenia. However, there are few interventions other than these that can be recommended for people affected.

The condition also tends to affect men more than women, and this is thought to be due to loss of testosterone as they age.

“Although sarcopenia can affect both men and women, my observations suggest that men might experience a higher prevalence of sarcopenia due to factors such as hormonal changes and decreased physical activity. Sarcopenia usually becomes problematic after the age of 50, but early signs of muscle weakness can be detectable before age 50, highlighting the importance of preventive measures. Advancing age is a primary risk factor for sarcopenia,” Dr. Takyrbashev said.

How metabolism affects sarcopenia and aging muscles

In this study, an international team of researchers looked specifically at the role of oxidized nicotinamide adenine dinucleotide (NAD+) levels, on sarcopenia.

NAD+ is a coenzyme involved in metabolism in all cells in eukaryotic organisms. It is involved in redox reactions in the Krebs cycle and glycolysis, for example. It is present in the mitochondria where it plays an important role in energy homeostasis.

Previous researchTrusted Source by these scientists had shown that low levels of it, along with lower mitochondrial energy production, were associated with greater skeletal muscle aging and sarcopenia.

Many members of the team are based at food-manufacturer Nestle-owned Nestle Research in Lausanne, Switzerland.

The researchers analyzed serum levels of 20 male Chinese individuals ages 65-79 with sarcopenia and age-matched healthy controls and found patients with sarcopenia had lower circulating concentrations of trigonelline, a chemical found in plants and animals.

Upon further analysis, the researchers found that trigonelline levels were positively associated with muscle mass, grip strength, and gait speed, and higher levels of NAD+ in skeletal muscle. They saw similar results in another cohort.

Tissue samples were exposed to trigonelline in vitro, and researchers found myotubes, a type of tissue found in the muscles, had raised NAD+ levels when treated with trigonelline, but other muscle cells, liver cells, and kidney cells did not. Treating muscle tissue samples from participants and aged-matched healthy controls with trigonelline raised NAD+ levels in both.

Worms were then treated with trigonelline on day one of adulthood and experienced an extended lifespan compared to controls. They also showed increased mitochondrial respiration.

The researchers gave male older (20 months old) mice a dietary supplement of trigonelline, and a 5-day course improved mitochondrial activity in the mice. A 12-week course of supplementation increased plasma, liver and muscle levels of trigonelline, compared to controls. Further experiments showed that grip strength increased in mice given trigonelline supplementation, compared to controls.

The authors suggest that the findings show that rather than changing the structure of muscle fibers, trigonelline improves mitochondrial activity in these cells.

How to increase levels of trigonelline in the body

The authors make the point that trigonelline is present in coffee and fenugreek. They cited research that shows that higher levels of caffeine are associated with lower levels of sarcopenia in Korea but said their own analysis showed this association is not found in the Middle East. They suggest this could be due to low coffee consumption there.

Nestle owns the Nescafe coffee brand.

A spokesperson from Nestle Research, Katharina Fischer, R&D Scientific Communications Manager told Medical News Today:

“Trigonelline is an endogenous metabolite both in women and men and NAD and mitochondrial metabolism are conserved between sexes. In this study, our work has mainly focused on male subjects for technical and clinical feasibility reasons, although some female subjects were also included in a small subset of the experiments. The conclusions of the study are therefore most likely applicable to both men and women.”

The researchers also found that dietary fiber and folate were associated with higher trigonelline levels in the body, and explained that the compound could also be made in the gut due to the actions of the microbiome.

“As reported in the paper, our clinical dietary modeling analysis identified links between dietary fiber and folate intake and trigonelline levels in the human body. While these signals open new opportunities to modulate endogenous trigonelline production, we focused the work on providing trigonelline orally given its high abundance in certain foods like fenugreek or coffee,” Fischer explained.

“The work opens new translational opportunities to test the clinical efficacy of increasing trigonelline consumption and to develop food products enriched in trigonelline for muscle health. The importance of maintaining NAD levels in other organs during aging also opens applications to other health benefits for healthy longevity,” she added.

Source - Medical News Today

How brain health at midlife may help predict cognitive decline in older age

• Researchers report that cognitive functioning in midlife might provide insights to brain health later in life.
• They say that staying physically healthy by adopting lifestyle habits such as not smoking, exercising regularly, eating properly, and participating in social activities can improve brain health.
• They note that keeping the cardiorespiratory system healthy is essential to brain health.

Cognitive function and health in midlife – ages 40 to 65 – might provide clues to brain health later in life, according to a reviewTrusted Source published today in the journal Trends in Neuroscience.

In their findings, researchers suggest that midlife is understudied and that more research should focus on this period in people’s lives.

During midlife, the brain undergoes significant molecular, cellular, and structural changes associated with cognitive decline, processes that accelerate during midlife.

Researchers say these individual changes could explain why cognitive aging varies from person to person.

During midlife, there can also be changes in the volume of structures within the brain. For example, the hippocampus, which is responsible for memory and learning, could shrink, altering those abilities.

“Two robust findings concerning the ‘middle-aging’ brain is the accelerating shrinkage of the hippocampus (a brain area critical for memory) and reduction in the volume of white matter (the connections between brain cells and brain areas), Yvonne Nolan, a professor of anatomy and neuroscience at the University of College Cork in Ireland and an author of the study, and Sebastian Dohm-Hanse, a PhD student at the university and an author of the study, told Medical News Today in a joint statement.

Changes in the midlife brain

Experts say that exploring changes in brain health in midlife and screening for risks of future cognitive decline could allow for earlier detection and treatment of diseases such as dementia.

Earlier treatment could also be more effective and give rise to additional approaches and treatment options.

“As the global population continues to age, there is a greater emphasis on optimization and primary prevention of brain health in the fields of geroscience and longevity,” said Dr. Mike Gorenchtein, a geriatrician at Northwell Lenox Hill Hospital in New York who was not involved in the study.

“A better understanding of these neurophysiologic pathways can potentially enhance screening and diagnosis of the initial stages of cognitive decline (before development of dementia), expand our knowledge of lifestyle interventions to optimize brain health, and pave the way for novel therapeutics for dementia,” Gorenchtein told Medical News Today.

Lifestyle factors, such as tobacco smoking, alcohol consumption, and diet, have been associated with brain aging.

Evidence suggests that changes in other parts of the body could predict brain health and function.

For example, the review notes that during midlife, changes in gait, reaction time, memory, white matter integrity, and neuroinflammation can accelerate. Experts say all of these could be tied to cognitive function in later years.

“This research is refreshing and empowers providers and their patients to take charge of brain health earlier rather than later,” said Shannel Kassis Elhelou, PsyD, a geropsychology and neuropsychology fellow at Pacific Neuroscience Institute’s Brain Wellness and Lifestyle Programs in California who was not involved in the study.

“Research on brain health in midlife is invaluable because it sheds light on critical factors influencing cognitive function and overall well-being during this pivotal stage of life,” Elhelou told Medical News Today. “Continued research in this area can lead to the development of targeted interventions and public health initiatives aimed at promoting optimal brain health.”

“Brain health in midlife can provide valuable insights to brain health later in life,” Elhelou added. “There is a growing body of research linking lifestyle choices and overall health to cognitive functioning in late life. Lifestyle habits developed during midlife, such as maintaining a healthy diet, exercise, sleep, stress management, and engaging in cognitively stimulating activities, can have long-term effects on brain health. Additional research has found factors associated with learning, such as higher levels of educational attainmentTrusted Source and more complex occupations with a lower risk for cognitive decline.”

The relationship between exercise and cognitive health

Exercise could aid in healthy cognitive aging, according to experts.

“Physical exercise during middle age has been found to slow the shrinking of the hippocampus and improve white matter connections,” Nolan and Dohm-Hanse shared with Medical News Today. “Running exercise, in particular, is beneficial for brain plasticity, especially as seen in animal studies. For instance, it is well known to increase the production of new brain cells in the hippocampus, which is critical for proper memory function. Improvements in memory have been found in both animals and humans following prolonged aerobic exercise.”

However, the researchers think that further research is still needed.

“Large meta-analyses of human exercise interventions, at least in the adult lifespan, have found mixed results concerning effects on cognitive function,” they said. “However, this could be because exercise intervention studies tend to be conducted very differently, so finding an average health-promoting effect among all studies is difficult, especially considering the changes that occur in brain structure and function throughout the lifespan.”

The relationship between exercise and cognitive health isn’t clear-cut.

For example, the researchers mention that a 2023 reviewTrusted Source of 24 meta-analyses found the effect of exercise on cognition was inconclusive and there was possible publication bias.

However, Nolan and Dohm-Hanse noted that “a physically active lifestyle should be promoted as it is known to have many beneficial effects throughout the body.”

“Future research with standardized designs will likely come to support that it is as good for the brain and mind as for the rest of the body,” they added.

Healthy aging

“It is without doubt that midlife offers the opportunity for true proactive primary prevention, although there is no universally accepted biomarker to stratify the risk of dementia in fully cognitively intact middle-aged individuals,” Dr. Mike Gorenchtein, a geriatrician at Northwell Lenox Hill Hospital in New York who was not involved in the study, told Medical News Today. “Midlife brain health can indeed, along with other important physiologic parameters, provide clues on projected cognitive health and overall health span, with many of these metrics still modifiable with lifestyle and (if indicated) treatment.”

The study authors note that the biological aging of organs in the body influences other organs’ aging. For example, the aging of the heart and lungs can affect the brain’s aging rate.

“If the cardiorespiratory system is in poor shape, it is likely that this will be detrimental to the brain – aging it faster, according to Nolan and Dohm-Hanse. “The health of the brain is intimately coupled to the health of the rest of the body, especially via the systemic circulation, so maintaining healthy blood pressure through physical activity, limiting alcohol intake and a healthy diet rich in fiber, omega-3 fatty acids and phytochemicals is important for healthy brain aging.”

“There is also some evidence to suggest that staying cognitively and socially active during the transition from middle to older age is beneficial for healthy brain aging,” they continued. “People who self-report spending a lot of time with friends and family and engaging in physical and mental activity tend to experience better mental and cognitive health. There is also evidence to suggest that a sense of purpose in life, such as deriving meaning from activities like work, volunteering, spiritual engagement, or creative activities, is linked with positive brain health outcomes.”

Source - Medical News Today

People under 65 may lower dementia risk with improved diet, lifestyle, other factors

 

• Young-onset dementia, also known as early-onset dementia, occurs when a person younger than 65 develops dementia.
• Researchers based in England and the Netherlands collaborated on a cohort study about young-onset dementia and focused on risk factors that could contribute to developing the disease.
• The scientists learned that 15 risk factors contribute to developing young-onset dementia, including diabetes, alcohol abuse disorder, and social isolation.

According to the Centers for Disease Control and Prevention (CDC), nearly 6 million adultsTrusted Source age 65 and older have Alzheimer’s disease (AD), the most common form of dementia, which is about 1 out of every 10 adults in this age bracket.

Many scientists prioritize dementia research, which includes finding medications to slow disease progression and learning more about changes people can make to reduce symptoms.

Researchers from the University of Exeter in England and Maastricht University in the Netherlands worked together to study young-onset dementia.

They focused their research on identifying risk factors for young-onset dementia and whether targeting these risk factors could reduce the risk of developing early dementia.

The research was recently published in JAMA NeurologyTrusted Source.

How common is early onset dementia?

Alzheimer’s Disease International projects dementia cases to increase from 55 million people worldwide in 2020 to 139 million people by 2050.

With such a staggering estimate, finding ways to identify factors that contribute to developing the disease is of utmost importance.

While young-onset dementia is rare, the CDC reportsTrusted Source that young-onset Alzheimer’s disease still affects around 200,000 people in the United States.

The researchers say that since most of the research into young-onset dementia focuses on genetics, they wanted to look more into how modifiable risk factors affect this form of dementia. Some modifiable risk factors include smoking, mental health, and alcohol intake.

The researchers used data from the U.K. Biobank for the study; the U.K. Biobank has nearly a half million participants who provide their genetic and other medical data. The purpose of the U.K. Biobank is to study health issues and make improvements in public health.

The scientists in the current project used data from nearly 356,000 participants who met the inclusion guidelines of being under age 65 and not having any form of dementia. Women comprised just over half (55.3%) of the participant pool.

The participants for U.K. Biobank underwent their initial assessments between 2006 and 2010 and followed up over the years, with the last follow-up in March of 2021.

Some information collected from the participants includes:

• biological samples
• socioeconomic status
• education
• alcohol or drug use
• psychiatric data
• environmental exposure to toxins
• general health information

After gathering information about the participants, the researchers analyzed the data to see whether there was an uptick in the incidence of young-onset dementia in people exposed to certain risk factors.

New risk factors linked to early-onset dementia

Throughout the follow-up period, 485 people developed young-onset dementia.

The researchers identified 39 risk factors, and after careful analysis, determined that 15 of these risk factors increased the risk of young-onset dementia.

Some of the newly-identified risk factors include:

• lower level of education
• alcohol use disorder
• social isolation
• vitamin D deficiency
• high C-reactive protein level
• depression
• stroke
• diabetes

“While further exploration of these risk factors is necessary to identify potential underlying mechanisms, addressing these modifiable factors may prove effective in mitigating the risk of developing [young onset dementia] and can be readily integrated in current dementia prevention initiatives,” the authors wrote.

The study findings show that staying on top of both mental and physical health is important, especially during mid-life.

Further, many risk factors are things people can take action on, such as expanding their social activities or asking their healthcare team to assess their vitamin D levels.

Early intervention key to preventing dementia, Alzheimer’s

Dr. David Merrill, a geriatric psychiatrist and director of the Pacific Neuroscience Institute’s Pacific Brain Health Center in Santa Monica, CA, spoke about the study with Medical News Today. Dr. Merrill weighed in on some of the risk factors the researchers identified.

When asked why depression could contribute to an increased risk for developing young-onset dementia, Dr. Merrill explained that “depression has both direct and indirect effects on brain structure and function.”

“We know that chronic depression can lead to more rapid loss of brain volume over time with aging,” Dr. Merrill noted. “Depression also tends to decrease levels of social and cognitive activities, which are themselves risks for cognitive decline.”

“Untreated depression can lead to progressively worsening cognitive decline, decline that may lessen or even stop if the depression is addressed,” he added.

Dr. Merrill touched on education level as a risk factor as well.

“[Socioeconomic status] and education level are developmental factors related to ‘cognitive reserve.’ Cognitive reserve can be thought of as the buffer against developing symptomatic dementia,” he said.

Dr. Allison B. Reiss, associate professor of medicine at NYU Long Island School of Medicine and part of the Alzheimer’s Foundation of America, also commented on the study to MNT:

“There are many things that can contribute to dementia that are in our environment and they are now more and more recognized,” noted Dr. Reiss. “The brain needs a very stable environment to function well and that includes many factors that are within our control or can be treated very well if the person receives good healthcare. The finding that genetics are not destiny is a hopeful one and indicates that we can take action to keep our brains at peak function starting in the younger years,” commented Dr. Reiss.

Dr. Reiss said that it is helpful for people to know there are things they can do to improve their chances of avoiding young-onset dementia.

“Diet, lifestyle, stress reduction, heart-healthy behaviors and seeking help for depression can make a difference,” pointed out Dr. Reiss.

“Improving financial status and making sure that people have enough to eat, safe housing and social connections does matter. It is important to see your healthcare provider regularly, follow recommended screening guidelines and work with that person or team to maintain overall good health.”

Source - Medical News Today        

Stress response linked to brain cell death in early-onset dementia

 

• A new study challenges the concept that protein aggregates in the brain are the direct cause of cell death in neurodegenerative diseases.
• The researchers noted the culprit is the body’s inability to turn off the stress response in brain cells.
• The findings highlight the potential for using certain drugs to deactivate the brain’s stress response and maintain the activity of a newly identified protein complex, SIFI.
• The new insights shift the focus from targeting protein aggregates to managing the stress response mechanism and introduce the potential for new treatment strategies.

Many neurodegenerative conditions, including Alzheimer’s disease (AD) and Parkinson’s disease (PD), have been linked to the buildup of protein aggregates in the brain, leading researchers to believe that these protein clumps are responsible for the death of brain cells.

As a result, efforts to find treatments focused on dissolving and eliminating these protein formations have largely been unsuccessful.

But now, new research published in NatureTrusted Source challenges this assumption.

The study authors propose the lethal factor for brain cells is not the protein aggregates themselves but the inability of the body to deactivate the stress response in these cells and maintain the activity of a newly identified protein complex known as SIFI.

Their study demonstrates that administering a drug that can halt this stress response can rescue cells affected by a neurodegenerative condition known as early-onset dementia.

Lead researcher Michael Rapé, PhD, professor and head of the Division of Molecular Therapeutics, Dr. K. Peter Hirth Chair of Cancer Biology at UC Berkeley, said this discovery opens up potential new ways to treat neurodegenerative diseases. He explained that we find clumps of proteins, known as aggregates, inside cells in certain diseases.

Prof. Rapé told Medical News Today the new research highlights how “a set of neurodegenerative diseases are connected through their persistent activation of a stress response pathway (the cellular stress response to mitochondrial import defects).”

“The stress response is normally turned off by a dedicated factor — the first example of ‘stress response silencing’ — and mutations in this factor cause early-onset dementia.”

— Prof. Michael Rapé, lead study author.

 How protein aggregates affect the stress response

Normally, cells can turn off their stress response after it’s no longer needed “by diverting the silencing factor (SIFI) from its stress response targets,” Prof. Rapé said.

However, in these diseases, the aggregates prevent the protein complex SIFI from doing its job, which means the cell’s stress response stays active when it shouldn’t.

The research has shown that we can help cells affected by these aggregates, such as those seen in early onset dementia, by using drugs to restore the normal process of turning off the stress response.

These treatments work even without removing the aggregates.

This finding is crucial because it suggests that the real danger from these aggregates is not the aggregates themselves but how they keep the stress response running.

Keeping the stress response constantly active can harm the cells, which might be a key factor in how these diseases progress.

Dr. David Merrill, PhD, board certified adult and geriatric psychiatrist and director of the Pacific Neuroscience Institute’s Pacific Brain Health Center in Santa Monica, CA, not involved in this research, told MNT that this research “represents a promising new way to treat otherwise incurable neurodegenerative diseases.”

“Turning off the stress response in cells that have otherwise lost that capability is a worthwhile approach to study,” Dr. Merrill explained.

Activated stress response leads to cell death

Diseases that might benefit from this finding include genetic conditions leading to ataxia, which is characterized by a loss of muscle control, as well as early-onset dementia.

The research also highlights that other neurodegenerative disorders, such as Mohr-Tranebjærg syndrome, childhood ataxia, and Leigh syndrome, exhibit similar overactive stress responses and share symptoms with the early-onset dementia studied.

The research team had previously believed that protein aggregates were directly lethal to neurons, perhaps by damaging internal cell structures.

However, their new insights reveal that these aggregates actually block the shutdown of a stress response that cells initially activate to manage malfunctioning proteins.

The perpetual activation of this stress response is what leads to cell death.

The team suggests that this mechanism could also be relevant to more prevalent diseases that feature widespread protein aggregation, like Alzheimer’s disease and frontotemporal dementia, although further research is necessary to explore the impact of stress signaling in these conditions.

Silencing the stress response

New treatment strategies could eventually involve “compounds that turn off the stress response kinase (HRI),” Prof. Rapé explained.

However, the “best way to treat neurodegenerative disease would be to limit aggregation and silence stress response signaling at the same time, reminiscent of combination therapy now in use in oncology,” the study author added.

Further research is needed, explained Dr. Merrill. “We need robust funding and rapid development of clinical trials targeting mechanisms like the one discovered in this work,” he noted.

“There is still much work to be done, but stress response silencing may prove to be a valuable way to slow or stop [the] progression of some neurodegenerative diseases,” Dr. Merrill concluded.

Source - Medical News Today

Scientists find new protein linked to early-onset dementia

 

• Scientists at the Medical Research Council (MRC) Laboratory of Molecular Biology in Cambridge, UK, have identified a novel protein called TAF15 forming aggregated structures in cases of frontotemporal dementia, challenging previous assumptions about the condition.
• This discovery is a novel addition to the limited set of proteins recognized for aggregating in neurodegenerative disorders like Alzheimer’s.
• This finding not only paves the way for advanced diagnostic tools and treatments but also raises the intriguing possibility that TAF15 may be linked to both frontotemporal dementia and motor neuron disease, shedding new light on these debilitating disorders.

Most neurodegenerative disorders, such as dementia, involve proteins clustering into filaments known as amyloids.

Novel protein may contribute to frontotemporal dementia

Frontotemporal dementia arises from the deterioration of the brain’s frontal and temporal lobes, which oversee emotions, personality, behavior, language comprehension and speech.

This condition typically manifests at an earlier age compared to Alzheimer’s disease, frequently being diagnosed in individuals between 45 and 65 years old. However, it can also present in individuals both younger and older.

In their new research, a team of scientists uncovered aggregated protein structures that may serve as a focal point for potential advancements in diagnostic assessments and therapies.

With the identification of the key protein and its structure, the researchers are now poised to focus on it to diagnose and treat this specific form of frontotemporal dementia.

This approach mirrors the strategies already in progress for targeting amyloid-beta and tau protein aggregates—hallmark features of Alzheimer’s disease.

Utilizing advanced cryo-electron microscopy to examine the brain

The scientists utilized advanced cryo-electron microscopy (cryo-EM) techniques to examine protein aggregates at an atomic level resolution in the brains of four individuals with this form of frontotemporal dementia.

Until now, scientists had assumed that a protein named FUS was responsible for aggregation in this type of dementia, drawing parallels with other neurodegenerative disorders.

Utilizing cryo-electron microscopy (cryo-EM), the MRC Laboratory of Molecular Biology scientists successfully determined that the protein aggregates found in each brain shared an identical atomic structure.

Surprisingly, the responsible protein was not FUS but another protein called TAF15.

The researchers clarified that this outcome was unexpected, as prior to this study, TAF15 had not been recognized for its role in forming amyloid filaments in neurodegenerative conditions, and no information about its structural characteristics existed.

Cryo-EM is revolutionizing our comprehension of the molecular mechanisms underlying dementia and neurodegenerative diseases in a broader context by providing insights that were previously unattainable with earlier technologies.

The researchers acknowledged that the intricate nature of conducting cryo-electron microscopy limited their examination to only four individuals’ brains.

Nevertheless, with our newfound knowledge of the pivotal protein and its structure, there is the prospect of creating tools for screening hundreds of patient samples to assess the extent of these abnormal protein aggregates.

In most cases, scientists have pinpointed the proteins responsible for this aggregation, enabling them to focus on these proteins for diagnostic assessments and therapies.

However, in approximately 10% of frontotemporal dementia cases, researchers had not yet determined the specific protein responsible.

Now, researchers have successfully identified the aggregated structures of the TAF15 protein in these particular cases.

The findings were published in NatureTrusted Source.

Frontotemporal dementia and motor neuron disease

Some individuals affected by frontotemporal dementia also experience motor neuron disease, a condition characterized by a progressive loss of muscle control.

In this investigation, two individuals who had both conditions donated their brains for study.

In these cases, the researchers detected the same aggregated form of the TAF15 protein in brain regions associated with motor neuron disease.

The presence of identical TAF15 aggregates in two individuals who had both frontotemporal dementia and signs of motor neuron disease raises the possibility that TAF15 may contribute to the development of both disorders.

Further research needed to investigate the impact of TAF15

The research team is currently examining whether these abnormal TAF15 aggregates are present in individuals with motor neuron disease who do not exhibit symptoms of frontotemporal dementia.

James Giordano, PhD, MPhil, Pellegrino Center Professor of Neurology and Biochemistry at Georgetown University Medical Center, not involved in this research, told Medical News Today that “this study further examined the possibility that additional abnormal proteins may be contributory to the neuropathological process of fronto temporal lobar degeneration and dementia (FTLD).”

“The study was well conducted and utilized a fairly broad sample of brain tissue taken from affected patients to evaluate the presence and extent of TAF protein, a variant abnormal protein constituent, which, together with other known abnormal proteins (such as characteristic tau and alpha-synuclein entities), are found in and contributory to the neurodegenerative processes of FTLD.”
— Dr. James Giordano

Dr. Giordano noted that “this study importantly, demonstrated that TAF protein is also present, albeit in somewhat lesser concentration, in the total proteinopathic constituency of the brains of these patients.”

Dr. Giordano noted that the study findings “further support and advance aspects of the amyloid hypothesis of neurodegenerative dementia.”

“Further, the identification of TAF variant may serve as an important diagnostic marker, as well as a potential therapeutic target in the treatment of FTLD,” he explained.

Jennifer Bramen, Ph.D., senior research scientist at the Pacific Neuroscience Institute in Santa Monica, CA, also not involved in this research,“frontotemporal lobe dementia (FTD) is an emotionally challenging disease with no cure.”

Dr. Bramen concluded that “FTD is a heterogenous disease, making it more challenging to research. A better understanding of different subtypes could ultimately lead to more treatment options for patients.”

Source - Medical News Today