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Evidence linking the development of Alzheimer’s disease to the toxic build-up of beta-amyloid protein in the brain was presented in a seminal study published in 2006. An assistant professor at Vanderbilt University recently made the suggestion that the authors of this study may have altered some of the images. What does all of this mean?

A specific beta-amyloid protein assembly in the brain impairs memory is the title of a 2006 study on dementia that was published in the journal Nature by a team of researchers from the University of Minnesota. According to the study, Alzheimer’s disease may be caused by a particular protein clump in the brain called beta-amyloid. The study demonstrated how these protein clumps, also referred to as amyloid plaques, may contribute to dementia using a mouse model.

The results of this study had a significant impact on the field of Alzheimer’s disease research. It has received more than 34,000 accesses and has been referenced in more than 2,200 scientific publications to date. According to a recent Science article, a Vanderbilt University assistant professor of neurology questions the validity of the 2006 Nature study’s findings, claiming that some of the images were altered.

What is image manipulation in peer-reviewed articles?
A photograph can be altered through the process of image manipulation. Dr. Elisabeth Bik, a microbiome and science integrity consultant at Harbers-Bik LLC, claims that it is simple to digitally edit photographs, such as when we remove a mole or wrinkle from a subject’s face in a portrait. It is forbidden to make any image modifications in scientific photography other than modest, overall contrast adjustments.

These days, the majority of journals expressly prohibit making any digital changes. However, it can be tempting and simple to digitally erase a stain or scratch from the background, add or remove cells, or alter the thickness of a protein band if an experiment is conducted and the results are not as clear or entirely different from what the researcher had anticipated. Performing some photoshopping is a far faster process than repeating the experiment.

It is not an unprecedented occurrence that the integrity of the visuals in a research study is doubted. Research conducted in 2016, of which Dr. Bik was a co-author, indicated that around 3.8% of scientific articles published in 40 journals between 1995 and 2014 contained images that could raise concerns, with around half of them hinting at intentional alteration.

What might this mean for dementia research?
Contacted Dr. Sylvain Lesné, an associate professor in the University of Minnesota’s neuroscience department, and Dr. Matthew Schrag, an assistant professor of neurology and director of the Cerebral Amyloid Angiopathy Clinic at Vanderbilt University, who has made the accusations against the 2006 Nature study. They didn’t reply to any of our inquiries. A public relations representative for the University of Minnesota said that the school is aware that concerns have been raised about specific images used in peer-reviewed research publications written by faculty members, and that they were going through the proper procedures to investigate any allegations made.

Given the impact of the 2006 Nature study on the field of Alzheimer’s disease research, Dr. Bik stated that additional evidence demonstrating image manipulation would be devastating to some research avenues. Lesné et al.’s Nature paper from 2006. has had a significant impact and inspired numerous researchers to repeat the study and explore the same hypothesis, she noted. Additionally, no clinical trials have been directly prompted by the AB*56 beta-amyloid work to date. However, it has sparked some additional research projects that have undergone clinical trials and taken slightly different approaches. However, Dr. Bik continued, that no experimental medication is effective against Alzheimer’s.

Dr. Bik commented It is fair to say that the 2006 Nature study has raised a lot of false hope in patients and led to a lot of wasted money and effort in research. There exist alternative theories to the beta-amyloid narrative, and it is possible that increased funding will be available to investigate them. Dr. But Grace Stutzmann, director of the Center for Neurodegenerative Disease and Therapeutics and professor and discipline chair of neuroscience at Rosaline Franklin University of Medicine and Science, told MNT that even if the purported intentional image manipulations in the 2006 Nature study were true, she did not believe this would call into question all of the previous research in the field.

She clarified that although many other amyloid variants have been investigated and replicated across multiple labs, this case only concerns a specific single arrangement of beta-amyloid from a single lab. In actuality, it’s akin to finding a needle in a haystack because the field of Alzheimer’s disease is very broad and encompasses more than just amyloid.

The head of research at Alzheimer’s Research UK, Dr. Sara Imarisio, claims that if these claims of image manipulation are accurate, research groups may have planned experiments after the study based on a false hypothesis, wasting valuable researcher time that could have been better used elsewhere. However, she noted that the paper’s results were highly specific and that, in contrast to some reports, they haven’t had a major impact on the advancement or course of Alzheimer’s research. Genuine findings will eventually come to dominate and direct the course of future studies, while findings that are impossible to replicate will be labeled as controversial and lose credibility even for research groups operating in this specific field.

Dr. Maria C. As we move forward, Carrillo, chief science officer at the Alzheimer’s Association, says it’s critical to remember that this investigation is limited to a small portion of Alzheimer’s and dementia research and does not represent the entirety of the body of science in the field. She continues, “Therefore, this should not impede the field’s swift pursuit of the underlying causes and other contributors to Alzheimer’s disease and other dementias.”. In an official statement, the Alzheimer Society of Canada expressed serious concerns about the allegations and called for further investigation. Scientific integrity is very important, and any possibility of wasting funds or time should be taken seriously.

What can journals do to prevent future misconduct?
Science, according to Dr. Charles Glabe, a professor of molecular biology and biochemistry at the University of California, Davis, depends on confidence and the knowledge that those who fabricate will eventually be exposed. Software tools that compare bands on a gel pixel by pixel were able to detect image duplication and copying, he said. This is all good, but fabricators will simply run a different gel and use that one instead of publishing the same band twice, knowing that it is easy to catch them copying bands. Furthermore, Dr. John Hardy, a professor at the UCL Queen sq. Institute of Neurology’s Department of Neurodegenerative Diseases and Reta Lila Weston Laboratories, informed MNT that preventing fraud is extremely challenging.

Image recognition software, which can now detect things that people had previously gotten away with, is one thing that has changed and was significant in this case, he said. This has meant quite a lot of ‘old fraud’ has now been caught like DNA testing of crime scenes. Going forward, Dr. Bik stated that scientific publishers should be more vigilant in ensuring that journals publishing research are checked for possible image manipulation. She recommended that scientific publishers invest time and resources in quality control of submitted articles. Despite their large profits, they aren’t screening manuscripts for fraud or other red flags.

They shouldn’t rely on unpaid peer reviewers who might not know how to look for misconduct; instead, they should hire specialists in statistics, ethics, and image forensics to screen such papers. Dr. Bik continued, “Journals and institutions should also penalize researchers who have been proven to have committed misconduct and retract papers much faster.”. A number of these worries regarding the Lesné papers were voiced years prior. There needs to be a change in how journals and institutions approach these issues; they are moving too slowly and warily.

References
https://www.medicalnewstoday.com/articles/alzheimers-study-controversy-what-does-it-mean-for-future-research?utm_source=ReadNext#What-can-journals-do-to-prevent-future-misconduct?

The Food and Drug Administration (FDA) has authorized a few new medications for treating Alzheimer’s disease since 2021, breaking a nearly two-decade hiatus. Targeting harmful protein aggregates in the brain, most of these medications are antibody therapies. Their endorsement has generated equal parts excitement and controversy. In this Special Feature, we look into the fundamental question of whether these medications are actually having an impact.

Alzheimer’s is a neurodegenerative illness that causes thinking, memory, and eventually the capacity to carry out daily tasks to gradually and irreversibly deteriorate. Since an aging population is the primary risk factor for Alzheimer’s disease, it has become a public health emergency. Globally, there were 57 million cases of Alzheimer’s disease in 2019, and by 2050, there are predicted to be 153 million cases. This emphasizes the necessity of developing disease-modifying therapies that alter the course of the illness permanently and slow its advancement.

However, attempts to create Alzheimer’s disease-modifying treatments have not been effective up until recently. The majority of clinical research aimed at creating Alzheimer’s disease-modifying treatments has concentrated on the beta-amyloid protein, whose aberrant build-up is widely thought to be the initial cause of this neurodegenerative condition. When the Food and Drug Administration (FDA) approved aducanumab, an antibody that targets amyloid-beta protein deposits, for the treatment of Alzheimer’s disease in 2021, it was regarded as the first disease-modifying medication for the illness.

However, aducanumab’s manufacturer, Biogen, announced that it would eventually stop selling the drug after the clinical trials did not yield consistent improvements in cognitive function. Since then, phase 3 clinical trials have shown that two additional anti-amyloid antibodies Biogen’s lecanemab and Eli Lily’s donanemab can slow the cognitive decline of people with early Alzheimer’s disease, and they have been approved by the FDA. Clinicians and researchers alike have greeted the approval of lecanemab and donanemab with enthusiasm, seeing it as a breakthrough after decades of clinical research having failed to yield effective disease-modifying therapies.

However, pointing to safety concerns and a lack of cost-effectiveness, some researchers have expressed concerns about the modest clinical benefits conferred by these anti-amyloid therapies. Dag Aarsland, even though there are obstacles in the fields of medicine, society, and clinical research, we must also acknowledge the advancements that have been made possible by the fact that, following years of expensive and fruitless research, we now possess clear proof of the possibility of slowing the advancement of the disease. The introduction of these medications may hasten the development of treatments and revolutionize clinical services for Alzheimer’s disease, the most common cause of dementia globally, according to Paresh Malhotra, PhD, who also noted that despite the anti-amyloid therapies’ modest efficacy, it is important to acknowledge that these drugs are the first to have clinical effects that appear to relate to a key mechanism of disease progression.

Based on the amyloid cascade theory, anti-amyloid antibody treatments like lecanemab and donanemab were developed. This theory states that the buildup of beta-amyloid protein causes additional alterations in the brain, ultimately resulting in the onset of Alzheimer’s disease. In particular, it is thought that the production of beta-amyloid aggregates causes oxidative stress, inflammation, neuronal damage, loss of synapses the “links between neurons that allow them to communicate” and, eventually, cognitive decline. This is supported by the fact that beta-amyloid protein buildup occurs several years before cognitive function, such as memory and decision-making, declines.

After secretase enzymes cleave a larger amyloid precursor protein, the beta-amyloid protein is produced. The units of the beta-amyloid protein are called monomers, and these monomers can combine to form oligomers, which are soluble short chains made up of two to more than fifty monomers. In addition to forming larger, soluble protofibrils and insoluble fibrils, beta-amyloid monomers can also aggregate. The extracellular space between the neurons is then populated by the assembled insoluble fibrils, which form plaques. It was previously believed that amyloid plaques were poisonous and caused Alzheimer’s disease to develop. Over the last twenty years, research has indicated that beta-amyloid oligomers may be more harmful than amyloid plaques and may have a greater role in the onset of Alzheimer’s disease.

It is believed that decreased beta-amyloid protein synthesis or clearance is the cause of the buildup of beta-amyloid aggregates. Over the last twenty years, some medications have been created that either target the enzymes responsible for producing beta-amyloid or help to clear beta-amyloid aggregates. However, because of their serious side effects or inability to have the intended clinical effects, these medications have not been approved by the FDA. The only FDA-approved treatments that target beta-amyloid aggregates are the anti-amyloid antibodies aducanumab, lecanemab, and donanemab. The affinity of these antibodies varies for different kinds of beta-amyloid protein aggregates. While aducanumab and lecanemab bind to plaques, protofibrils, and beta-amyloid oligomers, donanemab binds to a particular form of beta-amyloid that is exclusively present in plaques. Whereas aducanumab has a higher affinity for insoluble fibrils, lecanemab exhibits the highest affinity for beta-amyloid protofibrils.

Activating an immune response against beta-amyloid aggregates and subsequently removing them is one of the proposed mechanisms by which anti-amyloid antibodies produce their therapeutic effects. Additionally, anti-amyloid antibodies may bind to oligomers and neutralize them, or they may destabilize the plaques. Aducanumab was given accelerated approval by the FDA in 2021 to treat Alzheimer’s disease because of its capacity to remove amyloid plaques. Aducanumab’s effects on cognitive function varied throughout clinical trials, despite its success in removing amyloid plaques from the brain.

A lack of evidence to support aducanumab’s therapeutic effects led to controversy surrounding the FDA’s approval process and a reluctance among prescribers to administer the medication. Furthermore, as was already mentioned, Biogen has halted aducanumab’s development and sales as of 2024. On the other hand, lecanemab and donanemab have demonstrated the capacity to remove amyloid plaques while delaying the course of the illness. Patients with early-stage Alzheimer’s disease and lower baseline beta-amyloid levels respond better to these treatments.

Lecanemab and donanemab may now be administered intravenously to patients with early Alzheimer’s disease, including those with mild cognitive impairment or mild Alzheimer’s disease, according to FDA approval. Whereas donanemab must be given every four weeks, lecanemab is recommended to be given every two weeks. The ability for patients to stop taking donanemab treatment once total plaque clearance has been achieved is one of its special features. Amyloid plaques accumulate over some years, and it is thought that people may need only limited additional care. Lecanemab and donanemab phase 3 trial participants demonstrated a 27% and 36% slower decline in cognitive function when compared to placebo, respectively. On the other hand, some researchers contend that these results are negligible and similar to the effects of symptomatic treatments, like acetylcholinesterase inhibitors, which treat symptoms but do not alter the course of the illness.

Moreover, the Clinical Dementia Rating Sum of Boxes (CDR-SB) was used to quantify the cognitive alterations mentioned above. Additionally, when evaluating the effectiveness of these anti-amyloid therapies based on the absolute difference in decline in cognitive function between the placebo and anti-amyloid antibody treatment groups measured directly in terms of difference in scores on the CDR-SB scale researchers found that the impact was not clinically meaningful. The Mini-Mental State Examination [MMSE], one of the more objective measures of cognition, only showed a 14.8 percent slower decline in cognitive function in those receiving donanemab treatment. Put another way, it has been suggested that the data that is currently available indicates that these anti-amyloid medications may only offer a slight clinical benefit.

Dr. Espay went on to say that the case for exorbitant costs is made by the safety concerns combined with negligible clinical benefits. What is considered a clinically meaningful effect, however, is still up for debate. According to some researchers, the amyloid cascade theory is supported by the therapeutic advantages of anti-amyloid antibodies. Some, on the other hand, contend that there are still a lot of unanswered questions and that this conclusion is premature. The amyloid-beta hypothesis states that Alzheimer’s disease should have progressed more slowly as a result of aducanumab’s capacity to remove plaques. Opponents counter that while aducanumab effectively removed amyloid plaques in trials, there were inconsistent positive clinical outcomes. Comparably, in patients enrolled in the phase III trial, donanemab eliminated approximately 85% of plaques but only caused a 14.8 percent slower decline in cognitive function, as determined by MMSE scores.

Crucially, the amyloid cascade theory served as the foundation for the FDA’s decision to approve aducanumab. The buildup of the tau protein within neurons is another aspect of Alzheimer’s disease, and the degree of tau accumulation—rather than beta-amyloid accumulation is linked to the severity of cognitive decline. Pharmaceutical interventions that aim to lower beta-amyloid levels or its production are capitalizing on the notion that beta-amyloid is a key factor in the development and advancement of Alzheimer’s disease. This theory has received a lot of criticism. Additionally, these drugs’ clinical trial results show a low level of efficacy and a high level of risk.

Because of this, some researchers contend that the modest efficacy of anti-amyloid antibodies suggests that the beta-amyloid pathway contributes to the development of Alzheimer’s disease along with other pathways, rather than showing that the beta-amyloid pathway plays a focal role in the disease’s development. This theory contends that Alzheimer’s disease is also influenced by a complex web of variables, such as those connected to the environment, oxidative stress, inflammation, metabolic variables, and genes unrelated to the amyloid pathway. This perspective also suggests that anti-amyloid medications may be used in conjunction with other treatments to treat Alzheimer’s disease.

On the other hand, beta-amyloid aggregation might be a byproduct of other malfunctioning biological pathways or a downstream phenomenon. It is now evident that metabolic dysfunction upstream of amyloid plaque formation is crucial for the activation of the brain’s microglial cells, and this phenotypic shift reduces beta-amyloid degradation while simultaneously enhancing its formation, according to Perlmutter. Furthermore, two key characteristics of Alzheimer’s disease are synaptic degradation and neuronal viability being threatened by microglial activation. As a result, treatments that target brain metabolism will probably be very beneficial for Alzheimer’s disease, as early research employing GLP-1 agonists has now shown, continued Perlmutter.

Anti-amyloid antibody therapies have modest clinical benefits, but their risks, costs, and accessibility must be considered before pursuing them. A considerable percentage of participants in the phase 3 clinical trials for lecanemab (45%) and donanemab (89%), experienced adverse effects. For example, individuals receiving anti-amyloid antibody therapy frequently exhibit brain alterations referred to as amyloid-related imaging abnormalities (ARIA). These alterations, which are detected on routine follow-up magnetic resonance imaging (MRI) scans, involve either small areas of bleeding from blood vessel rupture (microhemorrhage) or brain swelling (edema).

For example, in phase 3 trials, ARIA was observed in 21% and 38%, respectively, of patients treated with lecanemab and donanemab. The majority of ARIA cases have no symptoms and go away in ten weeks. Although the majority of ARIA cases have mild to moderate symptoms, there have also been reports of severe side effects, including seizures and even death. For example, in the phase III donanemab clinical trial, approximately 16% of participants had severe adverse effects associated with ARIA, while the donanemab group had a 0 point35% death rate.

The long-term consequences of amyloid-related imaging abnormalities, even when they are mild to moderate in severity, are unknown, which raises concerns beyond these serious side effects. Adverse reactions like nausea, fever, rash, and dizziness are also linked to the infusion of these anti-amyloid antibodies. Reactions related to infusion were noted in 24.7% and 8.7%, respectively, of patients receiving lecanemab and donanemab treatment. Frequent magnetic resonance imaging scans and clinical follow-ups are necessary due to amyloid-related imaging abnormalities and other side effects. In the phase III trials for lecanemab and donanemab, people with at least one copy of the APOE4 gene—a gene associated with an elevated risk of Alzheimer’s disease were more likely to experience brain swelling.

Additionally, these medications were less effective in people who carried one or more copies of APOE4. Thus, before starting anti-amyloid therapy, people must undergo genetic screening. Anti-amyloid immunotherapies are also linked to a decrease in the volume of the entire brain combined with an increase in the volume of the brain’s ventricles, which are spaces filled with fluid. Reduced cognition is linked to an increase in ventricle volume and a decrease in whole brain volume.

It’s unclear, though, if these modifications in brain volume and cognitive function are causally related. Therefore, it is necessary to investigate the effects of these modifications in brain volume following anti-amyloid therapies. It’s interesting to note that the hippocampus, a part of the brain important for memory and learning, saw a lesser decrease in volume following donanemab therapy. The likelihood of a few Alzheimer’s patients in the general population meeting the requirements to be enrolled in lecanemab or donanemab clinical trials is low. These studies involved younger patients with fewer co-occurring medical conditions. Treatment for a real-world population of people with co-occurring conditions and Alzheimer’s disease is therefore likely to result in a higher rate of adverse events or lower efficacy.

The identification and diagnosis of patients who qualify for anti-amyloid therapies presents another difficulty for the healthcare system, in addition to managing side effects. The majority of Alzheimer’s patients do not receive a diagnosis until later in the illness, and to identify the disease early, many people would need to be screened using imaging scans or biomarkers of the cerebrospinal fluid. Therefore, widespread availability would require a significant financial outlay for the detection and diagnosis of early-stage Alzheimer’s disease, APOE4 genetic testing, and the tracking and treatment of ARIAs and infusion-related reactions, regardless of their severity.

Certain diagnostic tests are needed to confirm eligibility for new treatment, and in the UK, one-third of dementia patients do not receive a diagnosis at all. To make sure that those who qualify for new treatments can receive them when they’re most effective which seems to be in the early stages of Alzheimer’s disease investments in diagnostic infrastructure and workforce are required. Lecanemab infusions cost about $26,000, while donanemab infusions cost about $32,000 per year. The price of genetic testing, screening and diagnosis, and tracking and controlling side effects are not included in this, though. However, there is a chance that new biomarkers for tracking treatment outcomes and improvements in diagnostic techniques will lower costs and increase accessibility to anti-amyloid medications.

References:
https://www.medicalnewstoday.com/articles/alzheimers-are-newly-approved-drugs-making-a-real-life-difference#Amyloid-cascade-hypothesis-and-Alzheimers-research

The health benefits of fish oils have been the subject of numerous claims over the years. According to a new study, some people may be able to lower their risk of developing Alzheimer’s disease by taking fish oil supplements later in life. Fish oil supplements lowered the degeneration of brain nerve cells in older adults with a gene linked to an increased risk of Alzheimer’s disease, according to a small study. Larger clinical trials are recommended by experts to look into the advantages of omega-3 supplements for people who are at high risk of Alzheimer’s.

Since oily fish is a good source of omega-3 fatty acids (omega-3 PUFAs), it should be included in a healthy diet. Fish oil supplements, which are frequently promoted as having some health benefits, such as Heart and cardiovascular benefits; protecting eye health; healthy fetal development; memory, and other mental health benefits, are an option for those whose diet does not include oily fish. However, some of the health benefits of fish oils are debatable, and for certain individuals, using supplements may pose health risks.

A recent small study has revealed that older individuals with the APOEε4 gene, which raises the risk of Alzheimer’s disease, may benefit from taking fish oil supplements. According to the research, which was published in JAMA Network OpenTrusted Source, giving fish oil to individuals with the gene resulted in less breakdown of nerve cells; however, those without the gene did not significantly benefit from the treatment.

The possibility of individualized dietary interventions based on genetic predisposition is highlighted by this study. Although the results are encouraging, a more thorough investigation is required to fully comprehend the implications and provide firm guidelines. It’s also critical to keep researching additional dietary and lifestyle choices that may support cognitive health in senior citizens. “.

The Alzheimer’s Association states that a person’s risk of Alzheimer’s disease may be raised by some factors. These include genetics and family history; age; smoking; an unhealthy diet and/or being overweight; and a lack of exercise. Alzheimer’s disease has been linked to several genes, the most well-known of which is the APOE gene. A particular variation of this, APOEε4, raises the likelihood of Alzheimer’s disease, especially in people who receive APOEε4 from both parents.

Three soft gel fish oil capsules per day:
102 participants 75 years of age and older with comparatively low omega-3 fatty acid levels were included in the study. All of the participants had some degree of white matter lesions (common changes in the nerve cells of the brain in older people), but overall health was good, with no dementia (as determined by MRI scans at the beginning and the mini-mental state examination). Every day, the participants received three soft gel capsules containing 1 point 65 grams of omega-3 from the researchers. Three soft gels with only soybean oil were given to the control group; these gels had the same texture, taste, and smell as the omega-3 capsules.

Who was getting which treatment was a secret to both the participants and the researchers? Using MRI scans, the researchers tracked the progression of white matter lesions in each participant throughout the three-year trial. They also evaluated cognitive function.

Positive effects only in people with the APOEε4 gene:
There were no serious side effects from the treatment, and all participants tolerated it well. The investigators observed no statistically significant variation in the overall group’s results between the omega-3 treatment and placebo groups. Nonetheless, a notable distinction existed in the advancement of white matter lesions between the cohorts for individuals harboring the APOEε4 gene.

In comparison to individuals in the placebo group, those with the APOEε4 allele in the omega-3 group exhibited noticeably less breakdown of nerve cells. According to Allder, “Omega-3] PUFAs may have a different metabolic or inflammatory response compared to non-carriers, and carriers of the APOEε4 gene may have a higher risk of developing Alzheimer’s disease.” This is how the fish oils may have this effect. This gene is linked to oxidative stress and increased brain inflammation, both of which [Omega-3] PUFAs are known to reduce. “.

Fish oil may be a potential preventive treatment for some
The study’s authors suggest that while fish oil supplements may not be recommended for all older people, they may help lower the risk of Alzheimer’s disease in those who carry the APOEε4 allele. They do, however, stress that additional clinical trials are required to confirm their findings because this was a small study.

Our findings showed that over three years, there was not a statistically significant difference between the placebo and the group that took fish oil,” said Lynne Shinto, ND, MPH, senior co-author of the study and professor of neurology at OHSU School of Medicine, in a news release. She said, “I wouldn’t say you need to take fish oil to prevent dementia, but I don’t think it would be harmful.

Fish oils are generally safe, but people should only take them under medical advice, according to Allder and Molly Rapozo, RDN, registered dietician nutritionist and senior nutrition and health educator at Pacific Neuroscience Institute in Santa Monica, CA. “I always advise clients to consult with their medical team before adding supplements because contraindications are a serious concern. Although generally safe, there are effects based on age and dosage, particularly in individuals who have two copies of the APOE4 gene, Rapozo informed MNT. Increasing the amount of omega-3 in your diet is recommended, she continued, saying that you should “in the meantime, up your intake of small cold-water fish which are good sources of omega 3 fats.”.

REFERENCES:
https://www.medicalnewstoday.com/articles/fish-oil-benefit-people-high-risk-genes-alzheimers-disease
https://www.usnews.com/news/health-news/articles/2024-08-02/fish-oil-might-help-high-risk-older-adults-avoid-alzheimers
https://www.sciencedaily.com/releases/2024/08/240801121818.htm
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019002/

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The most prevalent type of dementia, Alzheimer’s disease, affects approximately 32 million people worldwide. Experts predict that the number of dementia cases will rise to 152 million by 2050 due to an aging population. Alzheimer’s disease currently has no known treatment options and no cure. Because of this, scientists have been working to develop new treatments for this kind of dementia. Immunotherapy, a treatment that strengthens the body’s immune response to combat Alzheimer’s disease, is one possible avenue of treatment that researchers are investigating.

The journal Science Translational Medicine published one of the most recent studies on immunotherapy for Alzheimer’s disease. Researchers from Washington University in St. Louis conducted this study. Louis describes how to use antibodies to help the immune cells in the nervous system remove unnecessary debris that can cause Alzheimer’s disease. Alzheimer’s disease currently has no known cure and current treatments only provide symptomatic relief.

The FDA [Food and Drug Administration] has approved lecanemab and aducanumab, two monoclonal antibodies, for treating Alzheimer’s disease. Clinical trials are being conducted on other monoclonal antibodies that activate the TREM2 receptor, thereby improving microglial responses to amyloid-beta pathology. However, more research is needed to determine how effective these treatments are. To improve overall efficacy, it is imperative to investigate alternative approaches that may prove to be more efficacious or serve as a supplement to currently available monoclonal antibody treatments.

The researchers used a mouse model to test their approach, which focused on proteins that control the activity of a particular type of immune cell in the nervous system called microglia. According to Colonna, microglia react to both activating and inhibitory cues from the surrounding tissue. Their main function is to eliminate poisonous substances that accumulate in the brain through phagocytosis, a process in which cells “consume” foreign substances. The signals that these toxins send cause microglia to engulf them.

The healthy components of the brain, which send signals to inhibit microglial activity, must be protected at the same time by microglia, he continued. Blocking inhibitory stimuli or supplying activating ones will both improve microglial phagocytic function. Receptors that reduce microglial phagocytosis are the main target of our strategy. Microglia may be able to reduce neuroinflammation and remove the harmful buildup of proteins like tau and beta-amyloid, which are linked to Alzheimer’s disease, according to earlier research.

Colonna and his colleagues also investigated the potential role of the brain microglia-resident LILRB4 receptorTrusted Source in the pathogenesis of Alzheimer’s disease. Brain microglia contain the receptor LILRB4, which binds to ApoETrusted Source, a fat-transporting protein that is both widely distributed in the brain and a component of amyloid plaques linked to Alzheimer’s disease. Alzheimer’s disease risk is elevated in certain human population variants of [the gene that expresses] ApoE. High levels of LILRB4 were first found on microglial surfaces in brain tissue samples from Alzheimer’s patients, according to research.

A mouse model that could express the human LILRB4 receptor was then employed by the scientists. It was demonstrated by their experiments that the microglia’s interaction with beta-amyloid plaques was interfered with by the LILRB4 receptor. Beta-amyloid accumulation in the brain was linked to behavioral changes in maze tests, but treatment with antibodies against LILRB4 resulted in decreased beta-amyloid levels in the brain and increased microglial activity.

We found that the ability of microglia to remove amyloid plaques is slowed down when ApoE binds to LILRB4, as Colonna explained. The capacity of microglia to remove these plaques is, however, increased when a particular antibody is used to prevent ApoE from attaching to LILRB4. This implies the possibility of amyloid plaque removal from Alzheimer’s patients treated with this antibody. Based on these results, we believe that administering this particular monoclonal antibody to patients with Alzheimer’s disease may aid in the brain’s removal of amyloid plaques and other toxic proteins that accumulate in neuron diseases. To improve the efficacy of other currently being tested treatments, this one may also be combined with them.

This study offers more proof of the potential of neuroimmunologyTrusted Source to treat and, eventually, cure Alzheimer’s disease, according to a board-certified neuropsychologist who was not involved in the research and who reviewed it for MNT. More evidence that monoclonal antibodies can disrupt the accumulation of beta-amyloid, one of the main disease biomarkers, comes from these research findings. She pointed out that we still don’t know how protection against cognitive decline and the progression of the disease is provided by reducing amyloid from this novel mechanism, anti-LILRB4 microglia signaling.

According to Sullivan, there will be a dramatic increase in the number of people with dementia as a result of the so-called “graying of the world.”. We must direct all available resources toward the treatment and medical management of these diseases because the substantial rise in the number of cases of neurodegenerative disorders has a huge financial and psychological cost. Toxins and other hazardous substances are kept out of the brain by the brain-protecting blood-brain barrier, which is maintained in part by microglia. This study outlines the potential consequences of disrupting these protective functions in the etiology (also known as the causal mechanisms) of Alzheimer’s disease, as well as potential treatments.

Effective Alzheimer’s disease treatment is still a goal of ours. One potential course of treatment would be to restore microglia function. The most prevalent type of dementia, affecting millions of people globally, is Alzheimer’s disease. Because of aging populations, it is anticipated that the number of cases will rise dramatically in the ensuing decades. It is a global public health emergency because it significantly increases the financial and caregiving load on families, communities, and society as a whole. According to the expert, there is currently no effective treatment that can halt or reverse the course of the disease. She continued, Our ongoing research suggests that multiple processes/risk factors may be involved in the development of Alzheimer’s disease. Investigating different therapies that can halt or slow down the neurodegenerative process is therefore crucial.

REFERENCES:
https://www.medicalnewstoday.com/articles/can-we-leverage-immunotherapy-against-alzheimers-disease
https://translationalneurodegeneration.biomedcentral.com/articles/10.1186/s40035-022-00292-3
https://molecularneurodegeneration.biomedcentral.com/articles/10.1186/1750-1326-8-36

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According to research, 22% of adults worldwide who are 50 years of age or older have Alzheimer’s disease at some point. Researchers are working to identify new markers for the early warning signs of this kind of dementia because it is anticipated that the number will rise. Alzheimer’s disease presently has no known cure, but some drugs can help delay the disease’s progression in its early stages.

Most people follow a certain pattern or routine of behaviors, including activity, every day. For instance, some people might move more in the evening and others might be more active in the morning. This is referred to as an individual’s daily activity pattern. A consistently high level of daily activity has been associated in previous research with a better cardiometabolic profile, which may help reduce an individual’s risk of cardiovascular disease. Regular daily activity patterns have also been connected by researchers to enhanced mental and physical health as well as better cognition in older adults. According to a May 2018 study, older men’s daily activity patterns may serve as predictive biomarkers for changes in sleep and cognitive function as well as clinically significant mortality outcomes. An increased mortality risk in older adults was linked to a more fragmented daily activity pattern, according to research published in October 2019.

In this investigation, scientists examined the information generated by an actigraph, a wristwatch-like gadget worn by eighty-two cognitively sound senior citizens who were a part of the long-running Baltimore Longitudinal Study of Aging. Actigraphs worn on the wrist have been the tool of choice for sleep researchers studying older adults’ sleep for decades, as stated. He pointed out that the accelerometer technology is generally the same as that found in widely used, commercial fitness trackers. My coworkers and I submitted an application for a grant from the National Institute on Aging (NIA) to investigate the relationship between Alzheimer’s disease and poor sleep, including the use of wrist actigraphs, because there is mounting evidence that sleep disturbances may raise the risk of the disease. This work is directly related to the grant that we were awarded.

There were discernible levels of the protein beta-amyloidTrusted Source in the brains of 82 research participants, whose average age was 76. Alzheimer’s disease is thought to be characterized by amyloid plaquesTrusted Source. The 25 amyloid-positive and 57 amyloid-negative participant groups differed significantly in terms of average afternoon activity and variability in activity throughout a larger time window, according to the researchers’ analysis of the actigraph device data. In the early afternoon, the scientists found that the average activity was higher in the amyloid-positive group.

Our findings are significant because, according to Dr. Spira, they demonstrated that, among individuals with cognitively normal brains, those with detectable levels of beta-amyloid exhibited distinct patterns of activity at specific times of the day compared to those without the protein. This is a new discovery. According to him, it will be crucial to monitor individuals who display activity patterns similar to those that we connected to the presence of beta-amyloid to determine whether they are more likely to experience cognitive decline in the future. It would be interesting to investigate if these 24-hour patterns can be used to predict the development of beta-amyloid in people without the condition.

In the future, I don’t see the clinical application of wearable recording technology, or “wrist actigraphy,” for the diagnosis of memory loss disorders such as Alzheimer’s dementia. It is common for people to become less active as they age, but other medical conditions like heart disease, neuropathies, or other medical issues are more concerning than dementia. Parkinson’s disease is a neurological movement disorder, and I would love to see this methodology used in its diagnosis.

REFERENCES:

https://www.medicalnewstoday.com/articles/mounjaro-zepbound-can-help-with-weight-loss-in-people-with-long-term-obesity
https://www.healthline.com/health-news/zepbound-weight-loss-questions-answered
https://agetechworld.co.uk/technology/wearable-device-could-provide-early-warning-of-alzheimers/?utm_source=rss&utm_medium=rss&utm_campaign=wearable-device-could-provide-early-warning-of-alzheimers&amp=1

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The active component of Viagra is sildenafil, which also serves as the foundation for the pulmonary arterial hypertension drug Revatio. According to a recent study, sildenafil may now be useful in the treatment of Alzheimer’s disease. Researchers, under the direction of the Cleveland Clinic, found that individuals taking sildenafil for pulmonary arterial hypertension or erectile dysfunction had a 30–54 percent lower incidence of Alzheimer’s disease than those who did not. In terms of dementia, Alzheimer’s disease is the most prevalent. According to estimates from the Alzheimer’s Association, roughly 6:07 million Americans have Alzheimer’s. It ranks as the nation’s fifth most common cause of death and as the population ages, it is anticipated to become more common. The Alzheimer’s Association reports that between 2000 and 2019, reported deaths from Alzheimer’s increased by more than 145%, while deaths from heart disease, stroke, and HIV declined.

Alzheimer’s disease is a progressive condition that worsens over time. It usually starts with memory loss and eventually causes problems interacting with others or reacting to one’s surroundings. The authors of the new study used computational models to parse the data for millions of patients in two medical databases, MarketScan Medicare Supplemental and Clinformatics. There has been a 54% decrease in Alzheimer’s cases in the MarketScan database. The Clinformatics database showed that to be thirty percent. After the data analysis, sildenafil was found to be a drug of interest, and laboratory research was conducted. Researchers who used brain samples from Alzheimer’s patients discovered that sildenafil reduced the amounts of neurotoxic tau proteins. These proteins accumulate in the brain as Alzheimer’s disease worsens. These tau proteins were long thought to be associated with amyloid plaques as potential causes of Alzheimer’s disease. However, the fundamental studies on amyloid plaques have been refuted. Neurotoxic tau proteins are still thought to be a key component of Alzheimer’s disease, despite this.

Additionally, they noticed that sildenafil-exposed neurons enhanced brain development and function, decreased inflammation, and altered metabolic processes linked to Alzheimer’s-related cognitive decline. Sildenafil is a phosphodiesterase type 5 inhibitor, or PDE 5 inhibitor, used to treat erectile dysfunction. PDE 5 inhibitors may be able to lower the risk of developing Alzheimer’s disease, according to a recent large-scale UK study. Still, there is no proof that these medications can treat the disease. The director of scientific programs at the Alzheimer’s Association, who was not involved in the new study, made this observation. Speaking about the current study, Dr. Dot Ismail stated that it is an observational study based on electronic healthcare records and that more research is necessary to determine the significance of the connection. A thorough investigation and carefully planned clinical trials are required before phosphodiesterase type 5 inhibitors are taken into consideration for the treatment of Alzheimer’s. According to Dr. Ismail, to definitively ascertain whether this class of medication can effectively treat Alzheimer’s disease, such trials would need to involve a diverse participant pool, including women.

He listed the lack of use of “gold standard” testing for Alzheimer’s diagnosis, such as imaging biomarkers and/or autopsy evaluation, as another significant study limitation. Dr. Neil Paulvin proposed that sildenafil may have an effect on Alzheimer’s by increasing blood flow and activating [the] part pathway. Gaining more insight into the mechanisms underlying the phosphatidylinositol 3-kinase (PI3K)/Akt pathway could potentially shed light on the processes involved in Alzheimer’s disease. This pathway is essential for many cellular functions and has been linked to cancer. One example of what could be possible with computer searches for useful molecules is the identification of sildenafil. Dr. Paulvin mentioned that these kinds of searches have produced medications like minocycline, which is used to treat bacterial infections, astaxanthin, an antioxidant, and gemfibrozil, which is used to control cholesterol. This study points to a possible new direction in drug repurposing. Because we already know a great deal about the safety and side effects of these treatments thanks to completed testing, repurposing current, approved treatments can be an important part of drug development. This can occasionally shorten the time and expense of the studies required for the new indication. However, he pointed out that Alzheimer’s is a particularly intricate and multidimensional illness. He pointed out that combination therapies that target various mechanisms are therefore probably required.

However, noted that it is frequently crucial to carry out fresh research over longer periods and in older subjects that represent the variety of people living with Alzheimer’s disease when thinking about repurposing an existing medication as an Alzheimer’s treatment. The Alzheimer’s Association Part The Cloud initiative, which has already contributed over $68 million to support 65 clinical trials, was mentioned by the speaker. Targeting both established and possibly undiscovered facets of the illness, these trials also aim to develop novel and repurposed therapies for dementia, including Alzheimer’s. He pointed out that the project is concentrating on various treatment avenues, including how immune responses impact brain alterations linked to Alzheimer’s disease, how brain cells use fuel and energy, how they clear debris from their structure, and how blood flow to the brain is preserved. Regarding sildenafil, Dr. Ismail emphasized that, in light of these preliminary findings, individuals should not use prescription drugs or over-the-counter [supplements and products similar to] phosphodiesterase type 5 inhibitors in the hopes of preventing Alzheimer’s or other forms of dementia.

REFERENCES:

https://www.medicalnewstoday.com/articles/sildenafil-viagra-may-help-reduce-alzheimers-risk
https://www.medscape.com/viewarticle/new-data-support-viagra-alzheimers-prevention-2024a10004md?form=fpf
https://fortune.com/well/2024/02/09/viagra-may-reduce-alzheimers-risk/https://www.theguardian.com/society/2024/feb/07/viagra-may-help-to-lower-the-risk-of-alzheimers-disease-study-finds

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On Friday, Eli Lilly declared that the U.S.S. committee headed by the Food and Drug Administration (FDA) was formed to assess donanemab, the Alzheimer’s medication whose approval was halted last year. Before the FDA decides whether to approve donanemab, the committee is anticipated to meet later this year. For many, though, the announcement is surprising. Donanemab significantly slowed the clinical progression of early Alzheimer’s patients in a trial conducted last year, but it also caused brain swelling and other side effects. Here are the opinions of experts on what this decision means for patients with Alzheimer’s disease. Lecanemab (Leqembi) and aducanumab (Aduhelm) are two of the three monoclonal antibody treatments for Alzheimer’s that include donanemab. Although there was little proof in the early trials that removing the amyloid plaques associated with Alzheimer’s disease slowed cognitive decline, all three medications function by doing so.

Over 55 million people worldwide suffer from dementia, and up to 70 percent of those cases are Alzheimer’s disease, which is defined by an accumulation of the proteins tau and amyloid. The U.S. approved aducanumab and lecanemab with accelerated approval. S. FDA, in response to encouraging clinical outcomes. As they were doing their due diligence on the medication, I believe they discovered a few aspects about it about which they wanted to form an advisory committee—basically, three things. There was a slight improvement in efficacy along with a slight rise in the safety signal. Donanemab had a very special, constrained dosing schedule regimen, with significant implications for clinical care. Additionally, tau imaging was utilized to gain entry into the trial. However, there was a question as to whether or not tau imaging would be required for clinical use in the real world and if it would be on the label. He clarified that careful monitoring would be necessary in the early stages of treatment, with MRIs performed in the first three to five months while possibly searching for ARIA or other indications that the drug should be stopped.

If they do occur, the drug is essentially stopped for a while, then the transfusion is resumed and stopped again for a while. However, in the case of homozygote APOE ε4 individuals who have two APOE ε4s and experience brain bleeding, hemorrhage, or edema as a result of the ARIA side effects, they may simply be stopped and not resumed, depending on the severity of those MRI findings. However, he feels that the risks are too great for him to suggest donanemab or any comparable medication. I do not think medications like donanemab are useful therapies for patients with Alzheimer’s dementia, as a clinical neurologist who treats and diagnoses patients with dementia. The risks of brain edema and bleeds associated with these medications outweigh their benefits. Like a lot of neurologists working in clinical practice, I refuse to take any drugs from [this] family. In the past, neurologists sold amyloid medications as a means of treating neuropathy symptoms; however, these drugs are no longer in use. I hope that the FDA’s decision to revoke Donanemab’s application is just one more step toward the discontinuation of [this] class of drugs.

REFERENCES:

https://www.medicalnewstoday.com/articles/fda-delays-approval-of-alzheimers-drug-donanemab-what-experts-think#Who-donanemab-might-not-be-right-for
https://www.healthline.com/health-news/fda-delays-approval-eli-lilly-alzheimers-drug
https://www.advisory.com/daily-briefing/2024/03/12/around-the-nation

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The identification of biomarkers for Alzheimer’s or Parkinson’s disease that can be found in bodily fluids like blood, urine, and saliva could aid in the discovery and development of new medications and therapies. Last year, a team of scientists created a wireless gadget that can identify SARS-CoV-2 strains in particular by detecting a very small number of molecules. They have now demonstrated that their gadget can be modified to identify chemicals connected to Parkinson’s and Alzheimer’s diseases. Researchers from the University of California, San Diego have demonstrated that their wireless, handheld device, which they developed to identify particular biomolecules, can also identify molecules linked to Parkinson’s and Alzheimer’s diseases. Initially, the instrument was designed to identify SARS-CoV-2, the virus responsible for COVID-19. Aptamers, which are brief strands of DNA or RNA that bind exclusively to particular molecules, are how it functions. Electrical energy can flow when binding occurs on the machine’s single-atom-thick graphene layer, producing a positive reading that verifies the presence of the molecule. In a previous study, it was demonstrated that their device could identify particular strains of the SARS-CoV-2 virus when very few viruses were present.

In their most recent study, this group of researchers demonstrated that their apparatus can identify various forms of tau and beta-amyloid, peptides that are characteristic of Alzheimer’s disease, as well as α-synuclein, a peptide that is present in higher concentrations in the brains of patients with Parkinson’s disease. To test the device’s capacity to identify these molecules, samples extracted from the autopsied brains of departed patients were used. The quantity of Americans who suffer from Alzheimer’s disease. S. may increase from 6.77 million to 13.78 million by 2060 if no major advancements are made in the field. While it has proven difficult to design clinical trials demonstrating the efficacy of drugs with cohorts of patients already exhibiting symptoms of the disease, breakthroughs are required not only in the diagnosis but also in the development of treatments. Currently, MRI, PET scanning, and neurocognitive testing are used in combination to detect Alzheimer’s disease, often after cognitive decline and other symptoms have started. The way that PET scans function is by looking for amyloid plaques, which are created when a peptide called beta-amyloid tangles with tau to form plaques. The cognitive decline that is observed in patients with Alzheimer’s disease is believed to be caused by these tangles interfering with nerve cell signaling in the brain.

The majority of studies concentrate on the existence, functions, and potential mechanisms of these peptides because Alzheimer’s disease patients’ brains have these plaques. Because these peptides are found in the brain, isolating them is still difficult and may require surgery. The findings of the study demonstrated that the apparatus the researchers had created could accurately and precisely identify several forms of these beta-amyloid peptides at low concentrations. Lead author Dr. Ratnesh Lal told Medical News Today in an interview, “What we saw in this paper is that the amount of beta-amyloid that goes into the brain in the saliva is almost 1,000 times more than what is the sensitivity of our system.”. He claimed that because there was no cross-reactivity to skew results, the device’s strength came from the electrical system’s sensitivity.

According to the paper’s authors, they plan to test the device’s ability to identify these molecules in blood plasma and cerebrospinal fluid before moving on to saliva and urine. Dr. Thomas K. Karikari, an assistant professor of psychiatry at the University of Pittsburgh who studies biomarkers for Alzheimer’s disease and was not involved in the research, stated that more research needs to be done to determine the best kind of biomarkers to detect Alzheimer’s disease in various types of body fluid. Standardized pathology tests on tau and amyloid present additional difficulties in obtaining consistent enough results to prevent false positives and negatives. Because amyloid is naturally very sticky, it can be challenging to separate and manipulate. Because of the blood-brain barrier, blood concentrations and concentrations in other tissues outside of the brain may not always reflect most changes observed in the brain. Dr. Karikari told  that his own research had looked at the phosphorylation patterns on Alzheimer’s specific tau-peptides to determine which specific molecules could be determined to have come from the brain and present in different concentrations in Alzheimer’s patients compared to a non-disease population. Put another way, you cannot tell if these biomarkers have come from the brain and not somewhere else in the body.

His earlier studies have demonstrated that tau binding is especially strong in the vicinity of the salivary gland. At the time, we demonstrated that there was no difference in saliva quality between the diagnostic group. Because tau in saliva would not always come from the brain, it was determined that tau in saliva was not a reliable biomarker for Alzheimer’s disease. “So we actually ended that at that point,” Dr. Karikari said. But now, he stated, “perhaps we can go back and be able to characterize the tau from the saliva much better,” since research has been done to identify the phosphorylation patterns on tau that define Alzheimer’s disease. “Dr. Less research has been done on urine, according to Karikari, and gathering urine from elderly patients who are incontinent presents unique difficulties. The device should be on the market in a year, according to the paper’s authors, who say they intend to apply for FDA approval in the next five to six months.

REFERENCES:

https://www.medicalnewstoday.com/articles/wireless-handheld-device-may-detect-alzheimers-parkinsons-biomarkers-early
https://newatlas.com/medical/portable-device-alzheimers-parkinsons-biomarkers/
https://www.altonmemorialhospital.org/Health-Library/View-Content?contentTypeId=6&contentId=2118881603
https://challenge.carleton.ca/parkinsons-alzheimers-early-detection/

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It has been discovered that higher concentrations of proteins that impair brain function are linked to visceral fat in the abdomen. According to researchers, creating metrics for visceral fat may help identify Alzheimer’s disease early on. According to experts, losing belly fat may help reduce the chance of getting Alzheimer’s. Adults in their middle years who have visceral fat around their internal organs in their abdomen may be more susceptible to Alzheimer’s. Based on research presented at the annual meeting of the Radiological Society of North America, having such fat deposits could cause changes in the brain related to Alzheimer’s up to 15 years before symptoms of the neurological disease appear — and as early as age 50. In this study, middle-aged people without any indications of cognitive problems were asked to participate in order to find correlations between high body mass index (BMI) scores, obesity, insulin resistance, and fatty abdominal tissue and amyloid and tau proteins, which are known to disrupt cellular communication in the brain.

Researchers at Washington University School of Medicine in St. Louis were led by Dr. Mahsa Dolatshahi, a post-doctoral research fellow at the Mallinckrodt Institute of Radiology (MIR). Louis, the brain region known to be affected early by amyloid pathology in Alzheimer’s disease, previously reported that a higher visceral to subcutaneous fat ratio in the belly was associated with a higher presence of amyloids in the precuneus cortex. According to those researchers, there was a correlation between elevated brain inflammation and higher levels of visceral fat. According to the new study, men are more likely than women to have belly fat and Alzheimer’s diseaseNo previous study has linked a specific type of fat to the actual Alzheimer’s disease protein in cognitively normal people, despite other studies linking BMI with brain atrophy or even a higher dementia risk, Dolatshahi stated in a press release. Comparable research has not looked into the distinct roles of visceral and subcutaneous fat, particularly in relation to the amyloid pathology of Alzheimer’s disease, as early as midlife. Dr. Mary Ellen Koran, an assistant professor of radiology and radiological sciences at Vanderbilt University Medical Center, said, It makes sense that visceral fat is linked to poorer brain health since we already know it’s linked to so many bad health outcomes, including heart health. But it’s important that we do the studies like these to define that link with evidence..

Visceral fat’s inflammatory secretions may lead to inflammation in the brain, one of the main mechanisms contributing to Alzheimer’s disease, according to DolatshahiWe don’t know whether this is a cause or effect—possibly an unhealthy lifestyle is linked to worse brain health in addition to more visceral fat, said Koran, a radiology expert who has identified Alzheimer’s disease. Before we can advance this clinically, more research in this area is necessary. For instance, she stated, It needs to be investigated because I don’t think we know what a ‘normal’ amount of visceral fat is. The results, according to researchers, may make it possible to identify Alzheimer’s disease early in an at-risk groupWe now have a uniquely better understanding of why this factor may increase risk for Alzheimer’s disease by moving beyond body mass index (BMI) in better characterizing the anatomical distribution of body fat on MRI, stated Dr. Cyrus Raji, senior study author, associate professor of radiology and neurology, and director of neuromagnetic resonance imaging at MIR.

According to Koran, the issue with utilizing BMI to evaluate health risks is that it ignores people who have a lot of muscle mass. Similarly, visceral and subcutaneous fat cannot be distinguished using waist circumference as a benchmark. Since visceral fat is known to be associated with a number of negative health outcomes, the expert suggested that alternative methods of assessing visceral fat be explored. Non-invasive imaging is a good fit for this purpose. Maybe in the future, we’ll be able to measure this using an inexpensive, radiation-free technique like ultrasound. According to the study, reducing belly fat may lower the risk of Alzheimer’s. According to Taylor Wilson, founder of Active Recovery Companions and an expert in nutrition and exercise, one strategy that has been proven effective in reducing belly fat is engaging in regular aerobic exercise, which includes activities like running, swimming, cycling, and dancing. These activities raise your heart rate and increase oxygen flow throughout your body. He told Medical News Today, Your body burns calories when you engage in aerobic exercise, including those stored in the belly area.Over time, a decrease in belly fat and overall weight loss may result from this calorie burn. Furthermore, studies have demonstrated that aerobic exercise significantly reduces belly fat in comparison to resistance training alone.

We know we can target fat with exercise and a healthy diet, but there are also new, effective drugs like Ozempic coming to market, Koran continued. However, more research is needed to determine how these medications affect visceral fat and brain function over the long run. Although the Food and Drug Administration has approved Ozempic and other comparable drugs for the treatment of type 2 diabetes, most of them still lack the necessary approval to be used for weight loss. Currently, some doctors are prescribing some of those medications off-label to help patients lose weight.

REFERENCES:

https://www.medicalnewstoday.com/articles/hidden-belly-fat-in-midlife-linked-to-alzheimers-disease
https://www.insideprecisionmedicine.com/topics/patient-care/hidden-belly-fat-linked-to-higher-alzheimers-risk/
https://neurosciencenews.com/midlife-visceral-fat-alzheimers-25235/
https://www.healthline.com/health-news/this-type-of-hidden-belly-fat-linked-to-higher-alzheimers-disease-risk

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