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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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Small blood vessel models are being grown in a lab to help researchers investigate the possible causes of cerebral small vessel disease. They stated that they hope to find viable treatments for the ailment, which can affect patients with type 2 diabetes and high blood pressure. Although the results are encouraging, experts warn that there is still much work to be done in this area of study. In order to determine what causes small blood vessel-like models to leak in people with specific medical conditions that raise the risk of vascular dementia and stroke, scientists at Cambridge University in England have grown the models in a lab. The journal Stem Cell Reports published the study’s findings today.

Small vessel disease (SVD) of the brain primarily occurs in two forms. The most prevalent usually affects people in their middle years and is linked to type 2 diabetes and elevated blood pressure. People in their mid-30s are typically found with the other rare form, which is inherited. A COL4 gene mutation is one of the causes. Researchers at Cambridge’s Victor Philip Dahdaleh Heart and Lung Research Institute used skin samples from patients suffering from a rare form of SVD brought on by COL4 gene mutations. Induced pluripotent stem cells, which can differentiate into nearly any type of cell in the body, were produced using these. By using these cells to create new cells, the researchers were able to model the disease that affects the brain vessels. The complex support system that surrounds cells, known as the extracellular matrix, was disrupted by the mutations in this particular form of SVD, according to the scientists. Tight junctions were especially affected by this disruption, which made the blood vessels leaky. The overproduction of molecules known as matrix metalloproteinases (MMPs), which are required to preserve the extracellular matrix’s structure, was also linked to the disturbance that the researchers saw. The group used medications that block MMPs to treat the cells. To do this, they employed the anti-cancer medication marimastat, the antibiotic doxycycline, or both. According to the researchers, blocking the MMPs with medication halted the leak and undid the harm. They did point out that these medications can have harmful side effects.

SVD patients are routinely treated by Dr. Sean Savitz, a professor and the director of the Institute for Stroke and Cerebrovascular Diseases at UTHealth Houston. He expressed his admiration for the study’s conclusions to Medical News Today, but he issued a warning, noting that the researchers only examined rare genetic mutation cases. This is a very well-done study that raises some interesting questions about the biological and molecular alterations that may be underlying some of the pathologies observed in brains affected by small vessel disease (SVD). Not involved in the study, Savitz stated, SVD is very common, especially in older patients with vascular risk factors. He continued, It’s very interesting to use skin cells to recapitulate the conditions in small vessel disease. The fact that a common antibiotic could undo some of the changes seen was intriguing. But we must remember that the patients from whom the cells were taken had uncommon genetic mutations.

According to the researchers, approximately half (45%) of dementia cases globally and roughly one-fifth of ischemic strokes are caused by SVD. These happen when the brain’s blood and oxygen supply are cut off by a blood clot. They represent the most prevalent kind of stroke. According to an article published in Advances in Clinical and Experimental Medicine, cerebral small vessel disease is the most prevalent, progressive, and chronic type of vascular disease. It impacts the capillaries, arterioles, and tiny veins that supply the brain’s deep structures, including the white matter. According to Dr. Shae Datta, director of cognitive neurology at NYU Langone Hospital—Long Island and co-director of NYU Langone’s Concussion Center in New York, SVD causes cognitive impairment, ischemic or hemorrhagic stroke, problems with mobility, and neuropsychiatric symptoms. Datta, who was not involved in the study, told Medical News Today that regular exercise, healthy diet, Mediterranean diet, folic acid, and vitamin B12 and avoiding adverse lifestyle factors like smoking, excess alcohol, or high dietary sodium, are all associated with having fewer SVD features in observational studies.

According to Dr. Catherine Arnold, a neurologist at Northwell Lenox Hill in New York who was not involved in the study, there are typically multiple coexisting conditions with SVD. These may obstruct the course of therapy. In an interview with Medical News Today, Arnold stated, The results of this study allow a better understanding of some of the potential mechanisms behind the development of small vessel disease (SVD) and potential mechanisms for future treatments. However, this study alone does not provide enough clarity or insight to change practice entirely, given the likelihood of multiple co-existing processes that contribute to the disease, the speaker continued. Future research is necessary to determine whether the findings hold true for the majority of patients with cerebral small vessel disease who also have vascular risk factors like diabetes and hypertension, according to Savitz. Therefore, the results of these experiments cannot be immediately applied to a clinical setting; however, the study lays the groundwork for particular future treatment development directions. Other than vascular risk factor modifications, which include blood pressure, glucose, cholesterol, and adherence to a healthy diet, we do not currently have any specific treatments.

Treating the underlying cause of a condition, such as an ischemic stroke, is often the first step in treatment. According to Morales, secondary prevention strategies often involve the use of statins, glycemic control, antihypertensives, antithrombotics, and other medications in addition to encouraging social interaction, a Mediterranean diet, and frequent exercise. Medication side effects can contribute to compliance issues, which can arise frequently. Is it effective? Evidence suggests that some of the effects and progression of vascular disease can be mitigated by our current strategies; however, more effective precision-based medical strategies that target these mechanistic pathways are clearly needed.

REFERENCES:

https://www.medicalnewstoday.com/articles/how-research-into-small-blood-vessels-may-help-prevent-stroke-vascular-dementia
https://www.port.ac.uk/news-events-and-blogs/news/tiny-blood-vessels-in-brain-could-be-key-to-treating-vascular-dementia
https://www.cam.ac.uk/research/news/lab-grown-small-blood-vessels-point-to-potential-treatment-for-major-cause-of-stroke-and-vascular

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The study, which was written up in the journal Current Biology, employed a computational model to delve deeper into the complexities of navigational errors that have already been linked to Alzheimer’s disease. Participants were divided into three groups by researchers, under the direction of Professor Neil Burgess and colleagues in the Space and Memory group* at the UCL Institute of Cognitive Neuroscience: healthy younger participants (a total of 31), healthy elderly participants (a total of 36), and patients with mild cognitive impairment (a total of 43). They then gave them a task to accomplish while using virtual reality goggles that enabled genuine motions. Participants in the trial followed a route that included two straight legs connected by a turn and was marked out by numbered cones. They then had to go alone back to where they had started.

The task was carried out under three different environmental conditions designed to test the participant’s navigational abilities: a virtual setting that remained intact, one in which all ground details were temporarily replaced with a plain texture, and one in which all landmarks were temporarily removed. The study’s findings revealed that patients with early Alzheimer’s regularly underestimated the number of turns along the route and shown greater directional unpredictability. The older participants who were in good health or those who had modest cognitive impairment, however, and who did not exhibit early indicators of Alzheimer’s disease, did not exhibit these particular abnormalities.

This may aid with diagnosis since it suggests that these navigational errors are unique to Alzheimer’s disease rather than an effect of normal aging or general cognitive loss. Dr. Andrea Castegnaro, co-first author and from the UCL Institute of Cognitive Neuroscience, stated that by focusing on particular navigational errors, their findings “offer a new avenue for the early diagnosis of Alzheimer’s disease.” We are aware that additional research is necessary to support these preliminary findings.

We work to create practical tests that are simple to incorporate into clinical settings while taking into account standard limitations like time and space. It can be difficult to achieve the standards of traditional navigation exams in a therapeutic setting. Our research focuses on particular navigational features that are better suited to these limitations.We are hoping to collect enough information for a trustworthy diagnosis in a time-effective manner by developing these tests to be both quick and comprehensive, boosting the chance of their general acceptance.

In the UK, there are reportedly 944,000 dementia sufferers, and Alzheimer’s disease is assumed to be the cause of more than 60% of cases. Similar predictions suggest that, barring medical advances, the number of Americans 65 and older who have Alzheimer’s disease could double, reaching 13.8 million by 2060. These patterns show the growing toll Alzheimer’s disease is taking on healthcare systems and society at large.

For improved disease management and therapy, early diagnosis is essential. Recent developments in blood testing can now identify amounts of tau and amyloid proteins that may indicate a possible Alzheimer’s disease, however these tests might not be enough on their own. According to Dr. Castegnaro, “Cognitive exams are still required to determine when the first cognitive impairments manifest, and existing spatial memory tests used in clinics frequently depend on verbal proficiency. Our tests are designed to provide a more useful tool that is independent of language or cultural context.

REFERENCES:

https://www.healthline.com/health-news/difficulty-walking-could-be-an-early-sign-of-alzheimers-disease
https://jnnp.bmj.com/content/75/2/196
https://www.ucl.ac.uk/news/2023/oct/certain-navigational-mistakes-could-be-early-signs-alzheimers-disease

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