Everything You Should Know About Chronic Traumatic Encephalopathy (CTE)

Chronic Traumatic Encephalopathy (CTE)

Chronic traumatic encephalopathy (CTE) is a degenerative and fatal brain disorder caused by repeated traumatic brain injuries (TBIs), such as concussions and head blows. It is also linked to the onset of dementia.

This disorder has an impact on how different parts of your brain function, communicate, and work with one another. CTE may have severe effects, depending on the level of damage and the affected parts of the brain.

CTE is well known to affect professional players in contact sports, including boxing, American football, and ice hockey. However, this syndrome can occur in those who have had recurrent head traumas, regardless of whether they play sports or not. Medical professionals also recognize it in veterans of the armed forces who have had several explosion- or blast-related incidents.

Who is affected by chronic traumatic encephalopathy?

A history of repetitive head trauma can cause chronic traumatic encephalopathy in any person. However, CTE does not emerge immediately. For most persons with this disorder, it might take years or decades before symptoms become severe enough to warrant attention.

Individuals who have repeated head injuries over an extended period are more likely to acquire CTE; this is especially true for professional athletes. A large percentage of people who play high school sports do not develop CTE. The typical age of patients with confirmed CTE falls between 42 and 43 years.

People with the highest risk include:

  • Individuals engaged in combat sports and competitions. It especially applies to traditional martial arts like judo, tae kwon do, aikido, boxing, and mixed martial arts (MMA).
  • People who participate in contact sports, such as ice hockey, football, and rugby.
  • People who participate in activities centered around roads and concrete, such as rollerblading, skateboarding, and cycling.
  • Military soldiers who are subjected to blasts and other concussive incidents.

How prevalent is chronic traumatic encephalopathy?

Experts are unsure how common CTE is, partly because there is no way to diagnose it while a person is still alive. Medical professionals may assume someone has it, but an autopsy is the only way to be sure. Also, many other degenerative brain disorders, including Alzheimer’s disease and frontotemporal dementia, have strong similarities and shared symptoms with CTE.

What are the symptoms of chronic traumatic encephalopathy?

The signs and symptoms of CTE typically appear gradually and worsen with time.

Typical signs and symptoms of CTE include:

Other signs that may manifest are:

  • Depression
  • Executive dysfunction
  • Difficulty speaking clearly
  • Tremors and other types of uncontrollable muscle movements (parkinsonism)
  • Balance issues and unsteady walking
  • Coordination loss (ataxia)
  • Increasingly aggressive behavior
  • Self-harming thoughts and actions (including suicidal thoughts and attempts)

What causes chronic traumatic encephalopathy?

CTE is the result of a combination of causes, which include:

  • A history of repeated head traumas: One of the most well-known risk factors for CTE is a history of repetitive head trauma. These impacts don’t necessarily cause someone to lose consciousness or be “knocked out.” Rather, repetitive head impacts have cumulative effects over time. That may result in the development of the condition.
  • Accumulation of fatty proteins in the brain: Another crucial factor in the development of CTE is the tau protein. Protein function depends on their structure. Similar to how a lock requires a key with the proper shape, your cells can only use a protein if it has the right shape. However, if a protein undergoes modifications, it will malfunction and may spread and impact other parts of the brain. Currently, the diagnosis of CTE involves locating a modified type of tau protein in a particular pattern within the brain.

How is chronic traumatic encephalopathy diagnosed?

There is no definitive way to diagnose CTE while an individual is alive. The only way to do so is to analyze brain samples under a microscope, which is only possible during a post-mortem examination.

Although a physician can make a tentative diagnosis of CTE based on your symptoms and a physical and neurological test, they may not be able to confirm the condition before death. In addition, they will go over your past head traumas and suggest particular laboratory and imaging testing. The most commonly used tests do not detect CTE. Instead, they rule out other possibilities. The tests include computed tomography (CT) scans, positron emission tomography (PET) scans, magnetic resonance imaging (MRI) scans, and cerebrospinal fluid (CSF) testing.

How is chronic traumatic encephalopathy treated?

CTE has no known treatment. Various factors, including your medical history, symptoms, and other conditions, may influence the treatments available for some symptoms. Furthermore, there are some practices that you can integrate into your lifestyle to promote overall brain health. Your healthcare professional is the best person to inform you of the treatments.

How can I prevent chronic traumatic encephalopathy?

Reducing the amount of head blows you might experience is the most effective method to lower your risk of CTE. Furthermore, there are easy methods that can lower your likelihood of experiencing a concussion, where impacts to the brain can produce significant symptoms:

  • Play safely: When participating in contact sports like ice hockey or American football, wear the proper protective gear. Helmets and other forms of protective gear can lower the risk of a concussion. Playing carefully and avoiding scenarios where you could experience a dangerous collision or put yourself in danger is also crucial.
  • Avoid playing while injured: If you receive a hit but retain your consciousness, it is easy to ignore it and consider yourself alright. A concussion can happen without unconsciousness, albeit it can be hazardous to take another blow after one has already occurred.
  • Wear your helmet: A helmet is essential for everyone who enjoys sports like skating, rollerblading, cycling, and related activities. They can significantly lower the incidence of concussions.
  • Wear your seatbelt: Nonathletes frequently sustain concussions as a result of traffic accidents. Wearing your seatbelt can lower your risks of getting a concussion or lessen the severity if you already have one.

References

  1. Chronic Traumatic Encephalopathy (CTE). Cleveland Clinic. https://my.clevelandclinic.org/health/diseases/17686-chronic-traumatic-encephalopathy-cte. Accessed: 30th April, 2024.
  2. Chronic Traumatic Encephalopathy (CTE). Alzheimer’s Association. https://www.alz.org/alzheimers-dementia/what-is-dementia/related_conditions/chronic-traumatic-encephalopathy. Accessed: 30th April, 2024.

A New Study Reveals that Viagra Reduces Alzheimer’s Risk by Over 50%

Viagra Reduces Alzheimer's Risk by Over 50%

A new study that supports some earlier findings implies that the erectile dysfunction medication Viagra may soon be recommended as a treatment to lower the risk of Alzheimer’s and aid in slowing the alarming global increase in dementia cases.

An unexpected contender has emerged in the decades-long and mostly unsuccessful search for medications to treat Alzheimer’s disease: the erectile dysfunction medication Viagra. A new study indicates that the small blue pill might also benefit our aging brains.

Researchers in the US have validated the medication’s potential to prevent vital proteins in nerve cells from tangling into a deadly mess by analyzing medical insurance data in conjunction with a laboratory investigation on the genetic and neurological effects of sildenafil, a drug commonly sold under the brand name Viagra.

Why Viagra may be associated with a reduced risk of dementia

Sildenafil (the generic name for Viagra) was never intended to be a drug for erectile dysfunction. Pfizer created the medicine to treat hypertension and angina [1]. The company was conducting clinical studies for sildenafil as a cardiac medicine when some patients experienced an unexpected side effect: erections.

Viagra belongs to a group of medications called PDE-5 drugs, or phosphodiesterase type 5 inhibitors. The medications dilate blood vessels and boost blood flow all over the body, including the penis. Since its discovery as a medication for erectile dysfunction, sildenafil has also been used to treat pulmonary arterial hypertension in both genders.

Research has shown time and time again that phosphodiesterase (PDE) inhibitors, an enzyme blocker class, not only increase penile blood flow but may also prevent dementia-causing neurodegeneration.

Considering that PDEs have been linked to nerve signaling pathways that affect neuroplasticity, this possibility may not come as a huge surprise. Previous studies on animal models have indicated that the PDE inhibitor sildenafil decreases excessive phosphorylation of ‘tau’ proteins in brain cells (which form toxic tangles), improving cognitive health and memory [2].

However, not all studies have found the same results; in fact, some have found no influence on the population level [3]. Furthermore, even if the medications might have a neurological impact, the underlying mechanisms are yet unclear.

Findings of the new research

In the new study, researchers in the United States mapped the metabolic and genetic activity underlying sildenafil’s therapeutic effects using cell cultures of neurons derived from stem cells donated by individuals with Alzheimer’s [4].

Following five days of treatment, the laboratory-grown neurons produced considerably lower quantities of tau proteins when extra phosphorus was introduced, indicating sildenafil’s ability to protect brain cells.

A reading of the messages that the cell’s DNA produced revealed numerous gene expression changes, many including inflammation, nerve communication breakdown, and nerve cell structure guidance.

While more research is required to determine the precise role that these subtle influences may play in the pathology of Alzheimer’s, knowing which primary gene families are impacted by sildenafil offers a good starting point for understanding how the drug functions and possibly why some brains develop Alzheimer’s in the first place.

The study’s second feature employed artificial intelligence to search for indications of sildenafil’s effectiveness at the population level.

Previous studies using medical insurance data discovered that sildenafil can reduce the risk of Alzheimer’s by approximately 60%. However, these depended on a single insurance database, potentially excluding elements that could lead to a different conclusion. Furthermore, it appears from these trials that patients receiving treatment for pulmonary hypertension (PH), or elevated blood pressure in the lungs, did not experience a similar decline in dementia risk.

In the recent study, the researchers included four routinely prescribed treatments for PH. They found that sildenafil also decreased risk in persons with pulmonary hypertension, in addition to verifying that it decreased Alzheimer’s risk by approximately 60%.

Feixiong Cheng, Cleveland Clinic biomedical informatician and co-first author of the study, stated that after computationally integrating this enormous amount of data, it was exciting to examine sildenafil’s effects on human neurons and real-world patient outcomes.

What’s next?

Cheng believes that their results give sufficient evidence for clinical trials to investigate the potential efficacy of sildenafil in Alzheimer’s patients.

Health officials may be able to quickly address the apparent rise in dementia if sildenafil can show that it is safe and effective in lowering the risk of Alzheimer’s disease, given that the FDA has already approved it for erectile dysfunction.

References

  1. Ghofrani, H.A., Osterloh, I.H. and Grimminger, F., 2006. Sildenafil: from angina to erectile dysfunction to pulmonary hypertension and beyond. Nature reviews Drug discovery, 5(8), pp.689-702.
  2. Cuadrado-Tejedor, M., Hervias, I., Ricobaraza, A. and Puerta, E., 2011. P´ erez-Roldán JM, Garćıa-Barroso C, et al. Sildenafil restores cognitive function without affecting β-amyloid burden in a mouse model of Alzheimer’s disease. British Journal of Pharmacology, 164(8), pp.2029-2041.
  3. NIH DREAM study finds Viagra and Cialis do not reduce risk of Alzheimer’s and related dementias. National Institutes of Health. https://www.nih.gov/news-events/news-releases/nih-dream-study-finds-viagra-cialis-do-not-reduce-risk-alzheimer-s-related-dementias. Published Online: 4th October, 2022. Accessed: 16th April, 2024.
  4. Gohel, D., Zhang, P., Gupta, A.K., Li, Y., Chiang, C.W., Li, L., Hou, Y., Pieper, A.A., Cummings, J. and Cheng, F., 2024. Sildenafil as a Candidate Drug for Alzheimer’s Disease: Real-World Patient Data Observation and Mechanistic Observations from Patient-Induced Pluripotent Stem Cell-Derived Neurons. Journal of Alzheimer’s Disease, (Preprint), pp.1-15.
  5. Huge Study Confirms Viagra Cuts Alzheimer’s Risk by Over 50%. Science Alert. https://www.sciencealert.com/huge-study-confirms-viagra-cuts-alzheimers-risk-by-over-50. Published Online: 25th March, 2024. AccessedL 16th April, 2024.

Fat build-up in brain cells may be responsible for Alzheimer’s: Study

Fat build-up in brain cells may be responsible for Alzheimer’s

Researchers have discovered evidence that fat deposition in brain cells may be the underlying cause of Alzheimer’s. Fat droplets seem to accumulate in brain immune cells as the major genetic risk factor for Alzheimer’s, suggesting an as-yet-unrecognized potential cause of the condition.

Alzheimer’s, which is characterized by neurodegeneration and progressive loss of mental skills, remains shrouded in mystery. The precise mechanisms of the disease remain unknown despite years of investigation. However, a recent study adds a new piece to the puzzle.

The accumulation of proteins in neurons has been the primary focus of research for the past few decades as the cause of Alzheimer’s. The formation of “plaques” and “tangles” in neurons is associated with the death of brain cells. Although scientists have recently developed drugs to remove these proteins, they are not the miracle cure that many people anticipated [1].

The function of lipid droplets in brain cells has drawn more attention lately. A team of neurologists, stem cell specialists, and molecular biologists from various American universities, under the direction of the Stanford University School of Medicine, have discovered evidence that suggests brain cell fat accumulation to be the underlying cause of Alzheimer’s. The journal Nature published the study [2].

The Link Between Alzheimer’s Risk Genes and Fat Droplets in the Brain

A recent study investigated the relationship between lipid droplets in microglia, the brain’s immune cells, and Alzheimer’s risk genes. The APOE gene has the strongest correlation with risk.

APOE plays a role in lipid processing, and in Alzheimer’s patients, the gene’s activity in microglia increases [3]. The cells accumulate lipid droplets as a result of APOE’s enhanced activity. However, whether this buildup is beneficial, benign, or hazardous has not been established.

The APOE gene exists in four variants, numbered 1–4, and one of them, APOE4, transports the most fat into brain cells, while APOE2 transports the least.

About the New Study

The researchers examined brain tissue from Alzheimer’s patients who passed away and from a control group that did not have the disease to conduct the study. They determined which genes are “turned on” by measuring gene expression within single cells.

The researchers wondered if the APOE variations had varying risks of acquiring Alzheimer’s disease. They carried out a few experiments to find out.

In the first experiment, scientists employed single-cell RNA sequencing to detect proteins within a test nerve cell. They applied their findings to tissue samples taken from patients who died from Alzheimer’s, who had two copies of either APOE4 or APOE3.

They discovered that the APOE4 gene was associated with an increased number of immune cells with a particular kind of enzyme that promoted the uptake of fat droplets into brain cells.

In another experiment, the team used cells from living individuals with either the APOE4 or APOE3 genotype to grow microglia in a dish. They discovered that adding amyloid to the brain cells of individuals, particularly with the APOE4 variant, caused the cells to accumulate fat more readily.

According to the researchers, the findings show that amyloid accumulation in the brain promotes the push of fat into brain cells, resulting in Alzheimer’s.

Potential for New Alzheimer’s Research

When considered collectively, the research raises the prospect of a novel theory about the pathophysiology of lipid droplets in Alzheimer’s disease.

According to Michael Haney, PhD, an assistant professor in the pathology department at the Perelman School of Medicine at the University of Pennsylvania and one of the study’s authors, the team believes that the protein accumulation typical to Alzheimer’s triggers the microglia to go into a pro-inflammatory state, which then causes the synthesis of lipid synthesis enzymes to be upregulated and lipid to accumulate in structures called lipid droplets [4].

Although lipid buildup in microglia is a novel discovery, researchers have observed this phenomenon before. According to Haney, it also happens outside of the brain when immune cells encounter microorganisms.

He added that they believe plaques cause a similar reaction in these brain immune cells, which causes lipid buildup and a pro-inflammatory, hazardous condition for these cells.

Can it be A New Step Towards Novel Alzheimer’s Treatment?

The authors of the current study believe that focusing on the role of fat accumulation will lead to novel approaches to treating Alzheimer’s in the future. Nevertheless, challenges prevail.

According to Haney, lipids and lipid-related proteins have significant functions outside the brain in processes you don’t want to interfere with, which makes it challenging to formulate drugs to target these lipids or the Alzheimer’s risk genes that transport lipids.

Put another way, he explained, they must figure out how to specifically target lipid buildup rather than lipids in general since doing so would lead to several additional issues.

However, Haney is optimistic as he believes this could be achievable with a deeper comprehension of how this accumulation particularly happens in microglia and what toxic substances they might be secreting.

Haney intends to carry on this line of work. He plans to conduct additional research to characterize the variety of illnesses in which microglia develop lipid droplets, how they build up these lipids, and how they may potentially damage neighboring neurons.

References

  1. Manly, J.J. and Deters, K.D., 2023. Donanemab for Alzheimer disease—who benefits and who is harmed?. JAMA.
  2. Haney, M.S., Pálovics, R., Munson, C.N., Long, C., Johansson, P.K., Yip, O., Dong, W., Rawat, E., West, E., Schlachetzki, J.C. and Tsai, A., 2024. APOE4/4 is linked to damaging lipid droplets in Alzheimer’s disease microglia. Nature, pp.1-8.
  3. Victor, M.B., Leary, N., Luna, X., Meharena, H.S., Scannail, A.N., Bozzelli, P.L., Samaan, G., Murdock, M.H., von Maydell, D., Effenberger, A.H. and Cerit, O., 2022. Lipid accumulation induced by APOE4 impairs microglial surveillance of neuronal-network activity. Cell Stem Cell, 29(8), pp.1197-1212.
  4. Newman, T. Alzheimer’s may be caused by a build-up of fat in brain cells. Medical News Today. https://www.medicalnewstoday.com/articles/alzheimers-may-be-caused-by-a-build-up-of-fat-in-brain-cells. Published Online: 21st March, 2024. Accessed: 4th April, 2024.
  5. Wilson, C. Alzheimer’s may be caused by a build-up of fat in brain cells. New Scientist. https://www.newscientist.com/article/2422090-alzheimers-may-be-caused-by-a-build-up-of-fat-in-brain-cells/. Published Online: 13th March, 2024. Accessed: 4th April, 2024.
  6. Yirka, B. Root cause of Alzheimer’s may be fat buildup in brain cells, research suggests. Medical Xpress. https://medicalxpress.com/news/2024-03-root-alzheimer-fat-buildup-brain.html. Published Online: 19th March, 2024. Accessed: 4th April, 2024.

How Type 2 Diabetes and Alzheimer’s Risk May be Related

Type 2 Diabetes and Alzheimer's Risk

A recent study found evidence that there is a link between type 2 diabetes and Alzheimer’s risk, which some health experts refer to as type 3 diabetes. Researchers said consuming a high-fat diet may boost inflammatory levels, increasing the risk of dementia.

Diabetes and Alzheimer’s are two of the most rapidly expanding health challenges worldwide. An estimated 1 in 10 individuals in the United States have diabetes, a condition that affects the body’s ability to turn food into energy [1]. Alzheimer’s is one of the top 10 most common causes of mortality in the US. It is a type of dementia that gradually impairs thinking and memory abilities.

Researchers from Texas A&M University presented their findings at the annual meeting of the American Society for Biochemistry and Molecular Biology, highlighting the emerging evidence that type 2 diabetes and Alzheimer’s disease are related.

They used mice to study the association between the two diseases; their results have not yet been published in a peer-reviewed journal [2]. The team traced a specific protein in the intestines to determine its impact on brain functions. They discovered that consuming a diet heavy in fat inhibits a protein known as jak3.

The absence of this protein caused inflammation in the mice, which started in the intestines and spread to the liver and brain. These mice showed Alzheimer’s-like symptoms, including cognitive impairment.

Possible relation between Alzheimer’s and type 2 diabetes

According to the study, controlling or preventing type 2 diabetes may help lower the risk of Alzheimer’s disease.

The scientists pointed out that earlier studies suggest that diet influences the development and severity of diabetes, and it has recently been linked to the risk of developing Alzheimer’s.

The study’s first author, Narendra Kumar, PhD, an associate professor of pharmaceutical sciences at Texas A&M, said that meta-analytic statistics show that people with type 2 diabetes had a 56% higher risk of developing Alzheimer’s disease dementia [3].

Since there is a recognized connection between type 2 diabetes and diet, the researchers believe that lifestyle and diet may be some of the primary factors influencing Alzheimer’s development.

Kumar thinks it’s probable that this connection would hold for different forms of dementia, even though this study hasn’t looked into it, and it is too soon to reach that conclusion.

How a leaky gut could play a role

According to Texas A&M researchers, the jak3 protein can cause a leaky gut, resulting in low-grade chronic inflammation, type 2 diabetes, diminished ability in the brain to eliminate harmful compounds, and dementia-like symptoms.

A leaky gut is a disorder in which intestinal wall gaps allow toxins and microbes to leak out and enter the bloodstream. Not all health professionals acknowledge this as a separate medical disease, and it needs more research.

The researchers believe that adopting a nutritious diet and regulating blood sugar can help stop this process and inflammation. Healthy food and lifestyle practices should ideally start early enough to prevent high blood sugar or, at the very least, early enough to reverse prediabetes.

According to the researchers, these modifications may lower the risk of Alzheimer’s and type 2 diabetes.

Linking type 2 diabetes with Alzheimer’s

Approximately 81% of individuals with Alzheimer’s also have type 2 diabetes, per a study from USC’s Keck School of Medicine [4]. The dementia risk correlated with the age of diabetes diagnosis: the younger the age of developing diabetes, the higher the chance of developing dementia.

Scientists have labeled the combination of these two illnesses as “type 3 diabetes.” According to the researchers, the liver may play a crucial role in the gut-brain connection since it metabolizes food.

Experts know that excessive blood sugar or insulin can damage the brain and raise the chance of Alzheimer’s, yet the exact cause of this disorder is still unknown [5].

The brain uses half of the body’s sugar energy to function effectively, making it the organ with the highest energy requirements. The Centers for Disease Control and Prevention state that blood vessels in the brain can sustain damage from both high and low blood sugar levels [6].

An abnormal blood sugar level may damage brain blood vessels and nerves, which can lead to issues with mood, memory, learning, weight gain, and hormonal fluctuations. It may eventually result in Alzheimer’s disease.

Changing lifestyle may help

Experts believe that lifestyle factors such as exercise, diet, and others are equally significant. Diet and lifestyle modifications to manage weight are beneficial in lowering and controlling diabetes risk. Numerous people find immense relief from their disease with the introduction of new and advanced medications. However, there are many other things people can do to manage their condition on their own.

In particular, those with prediabetes may benefit from changing their lifestyles to reverse the condition, prevent Type 2 diabetes from developing, and maybe lower their risk of Alzheimer’s.

References

  1. Type 2 Diabetes. Centers for Disease Control and Prevention. https://www.cdc.gov/diabetes/basics/type2.html. Accessed: 2nd April, 2024.
  2. Study Links Diet, Diabetes, and Alzheimer’s. Neuroscience. https://neurosciencenews.com/diet-diabetes-dementia-25802/. Published Online: 23rd March, 2024. Accessed: 2nd April, 2024.
  3. Cholerton, B., Baker, L.D., Montine, T.J. and Craft, S., 2016. Type 2 diabetes, cognition, and dementia in older adults: toward a precision health approach. Diabetes Spectrum, 29(4), pp.210-219.
  4. A growing body of research links type 2 diabetes with risk for Alzheimer’s. Press Release, Keck School of Medicine of USC. https://keck.usc.edu/news/a-growing-body-of-research-links-type-2-diabetes-with-risk-for-alzheimers/. Published Online: 16th March, 2022. Accessed: 2nd April, 2024.
  5. Diabetes and cognitive decline. Alzheimer’s Association. https://www.alz.org/media/documents/alzheimers-dementia-diabetes-cognitive-decline-ts.pdf. Updated: February, 2023. Accessed: 2nd April, 2024.
  6. The Effects of Diabetes on the Brain. Centers for Disease Control and Prevention. https://www.cdc.gov/diabetes/library/features/diabetes-and-your-brain.html. Accessed: 2nd April, 2024.
  7. How type 2 diabetes may be linked to Alzheimer’s disease risk. Medical News Today. https://www.medicalnewstoday.com/articles/how-type-2-diabetes-may-be-linked-to-alzheimers-disease-risk. Published Online: 23rd MArch, 2024. Accessed: 2nd April, 2024.