Advanced searches left 3/3
Search only database of 8 mil and more summaries

New Research On Alzheimer Disease

Summarized by PlexPage
Last Updated: 20 October 2020

* If you want to update the article please login/register

General | Latest Info

As the most common form of Dementia and the sixth - leading cause of death in the US, Alzheimer's Disease is not foreign to Americans. Many in the US know someone battling a disease or disease that doctors are still continuing to understand. While the majority of previous research has been focused on treatment, researchers are beginning to shift their attention toward prevention. In recent virtual presentation in partnership between Alzheimers Associations Michigan chapter and Michigan Alzheimers Disease Research Center, Bruno Giordani, ph. D, professor in departments of psychiatry, neurology and psychology, discussed science behind Alzheimers Disease as well as the latest research from the most recent Alzheimers Association International Conference. According to Giordani, new research findings lead to an entire change in emphasis of research, as more evidence was released to support risk - reducing tactics over later treatment. Alzheimer's Disease involves memory loss, confusion and spatial difficulties, which all come down to the existence of amyloid plaques. Amyloid plaques, or hallmarks of Alzheimer's Disease, as Giordani calls them, are clumps of misshapen proteins that form between nerve cells and essentially act as roadblocks for memory. Cell death also occurs in specific areas of the brain, such as the hippocampus, which is critical for areas of cognition like memory and spatial navigation. Scientists are gaining better understanding of the course of Alzheimer's Disease, which progresses from prodromal or pre - clinical period to mild cognitive impairment and then Dementia. Knowledge of this path, as well as earlier tracking of amyloid, has given doctors the chance to work toward risk diagnosis and preventative medications, as opposed to later treatment of disease. Id usually tell you about all the exciting new amyloid drugs present at AAIC meeting; amyloid busters that we can apply to get rid of amyloid in the brain. Frankly, these have not worked out as expect, Giordani explain. Researchers are now attempting to disrupt the process even earlier, before amyloid plaques form and begin to disturb memory. In recent discussion with Giordani, he highlighted news that Biogen, American biotechnology company, completed submission to the US Food and Drug Administration for review of aducanumab, investigational treatment for Alzheimer's Disease that targets amyloid in the brain in hopes of reducing its buildup. If approve, aducanumab would become the first therapy to reduce clinical decline of Alzheimer's Disease and would also be the first therapy to demonstrate that removing amyloid beta results in better clinical outcomes, which could be significant news for Alzheimer's treatment. Researchers are also examining how parts of the body, other than the brain, may play a role in disease development. Studies have looked into the effect of various medications individuals are already taking, such as insulin, and are finding promising results. Study looking at inhaled insulin show some cognitive and amyloid - tau distribution improvements, but the type of inhaler seems to make a big difference. Other approaches include studying gingivitis and other markers of inflammation, which Giordani says may help track disease process earlier on as well.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

The hope for future drugs

Finding out if you or your loved one has Alzheimer's Disease can be difficult, confusing and scary. Fortunately, future is looking brighter as researchers and organizations like the Alzheimers Association work towards finding a cure. Learn more about disease, what preventative measures you can take, and current therapies being Study. First discovered by Dr. Alois Alzheimer in 1906, Alzheimer's Disease is a type of Dementia that causes issues with memory, thinking and behavior. Typically, symptoms develop and worsen over time, eventually becoming severe enough to interfere with daily tasks. There is not one single cause of Alzheimers, but risk factors include: age - people tend to develop Alzheimers at age 65 and older. Family history - if you have an immediate family member with a disease, youre more likely to develop it yourself. Genetics - Certain genes, like apolipoprotein E, are linked to Alzheimer's Disease. While there is currently no known cure for Alzheimer's Disease, there are medications or other treatments doctors can recommend in order to help ease symptoms and delay progression of the disease. At present, there are five Alzheimer's drugs approved by the US Food and Drug Administration to treat symptoms of the disease, but they do not treat its cause or progression. There are no known methods of preventing disease. However, researchers have focused on overall healthy lifestyle choices as a way to prevent decline, including: quitting smoking Regular exercise Cognitive training exercise Plant - base diet Consume antioxidants Interact socially we use Life Stations at Edgewood to help our residents spark old memories and create activities that encourage interest, movement and interaction. Make up of old gardening supplies, baby dolls and other items, these stations help residents revisit and retain memories while also inspiring new moments of joy. The next generation of drug therapies is under research, and they give some hope for the future of preventing and curing Alzheimer's Disease. The following are examples of medications being analyze:

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Alzheimer's prevention trials

Clinical Trials are research studies conducted with human volunteers to determine whether treatments are safe and effective. Without clinical research and the help of participants, there can be no treatments, prevention or cure for Alzheimer's Disease. Treatment Trials to test new drug and non - drug based dementia treatments or combinations of treatments. Diagnostic studies that find new tests or procedures for diagnosing disease or condition. Prevention Trials that investigate ways to prevent Onset of diseases. Quality of life studies that explore ways to improve the quality of life for individuals who have chronic illness, their caregivers and family members. Online studies, which are web - base research conducted entirely online.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Summary

Alzheimer's Disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, ability to carry out the simplest tasks. Most people with diseasethose with late - onset type symptoms first appear in their mid - 60s. Early - onset Alzheimers occur between people's 30s and mid - 60s and are very rare. Alzheimer's Disease is the most common cause of Dementia among older adults. The disease is named after Dr. Alois Alzheimer. In 1906, Dr. Alzheimer noticed changes in brain tissue of a woman who had died of an unusual mental illness. Her symptoms include memory loss, language problems, and unpredictable behavior. After she die, he examines her brain and finds many abnormal clumps and tangled bundles of fibers. These plaques and tangles in the brain are still considered some of the main features of Alzheimer's Disease. Another feature is loss of connections between nerve cells in the brain. Neurons transmit messages between different parts of the brain, and from the brain to muscles and organs in the body. Many other complex brain changes are thought to play a role in Alzheimers, too. This damage initially appeared to take place in the hippocampus, part of the brain essential in forming memories. As neurons die, additional parts of the brain are affect. By final stage of Alzheimers, damage is widespread, and brain tissue has shrunken significantly.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Important Breakthroughs

Investigators at Case Western Reserve University School of Medicine identified a previously unknown gene and resultant protein that may potentially slow the progress of Alzheimer's Disease. The team has named protein aggregatin and they believe that if gene or protein could be suppress, it could possibly slow development of disease. Base on data we have, this protein could be an unrecognized new risk factor for Alzheimer's Disease, said Xinglong Wang, associate Professor of pathology at Case Western. We also see this as a potential novel therapeutic target for this devastating disease. Which is all very early in any development phase. The research team, led by Wang and Xiaofeng Zhu, Professor of Population and Quantitative Health Sciences at Case Western, has filed a patent via the universitys Office of Research and Technology Management for novel Alzheimers Disease treatments and diagnosis based on this and related study, according to Wang. The research was published in the journal Nature Communications. Alzheimer's Disease is marked by accumulation of amyloid plaques in the brain. Another abnormal protein, tau, is also associated with disease, which results in loss of memory and cognition. The newly identified gene is FAM222A, which researchers associate with imaging genetics to AD - related regional brain atrophy. Protein, aggregatin, that gene codes for is mostly expressed in the central nervous system and is increased in the brains of AD patients as well as in AD mouse model. Aggregatin accumulates inside amyloid deposits, and the way it physically interacts with beta - amyloid, helps accumulation of beta - amyloid. This protein characteristically accumulate, or aggregates, within the center of plaque in AD patients, like the yolk of an eggwhich, is part of the reason we name it aggregatin, Wang say. Research was supported by grants from the National Institutes of Health and Alzheimers Association. The Alzheimers Disease Neuroimaging Initiative supplies genomic and brain imaging data, which is also supported by NIH. The so - called amyloid theory of Alzheimer's Disease has been under fire in recent years. Although it is clear that accumulation of amyloids in the brain is related to disease, dozens of drugs that clear or prevent amyloid accumulation fail to improve cognitive symptoms of disease muddy waters. Currently, theory has regained at least some support with Biogens aducanumab. The drug failed clinical trial in March 2019, but further analysis of data at higher dose suggests it actually work, and will soon be submitted to the US Food and Drug Administration, although there is still quite a bit of skepticism among scientists about the effectiveness of drugs. Perhaps more realistically, many researchers believe that amyloid and tau are only part of story, and that other factors, some unknown, and others likely related to neuroinflammation, are important. Although it is not completely understood how amyloid - beta leads to plaque formation, this new research appears to shed some light on the subject.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

JAX innovations

Tufts CTSI, together with Jackson Laboratory, is hosting a Team Science Summit: Innovations in Alzheimers and Healthy Aging Research on Wednesday, September 18, 8: 00AM - 3: 30PM, at Jean Mayer USDA Human Nutrition Research Center on Aging. This event will bring together researchers and clinicians from across Tufts University and Tufts CTSI partners to explore opportunities for multidisciplinary collaborations focus on neurodegenerative Disease and Healthy Aging Research. Presentations will focus on ongoing work to interrogate mechanisms of disease evolution, build novel Disease Models and translational tools, and enable biomarker - drive Precision Medicine approaches for care and disease prevention. We encourage clinicians and researchers with an interest in forming new collaborative research projects, including postdocs, to register and attend this full - day event consisting of panel discussions, poster presentations, and networking opportunities.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

From mouse to man

In the past three decades, scientists ' knowledge of the biology that underlies Alzheimer's Disease has advanced tremendously. In particular, roles of aberrant accumulation in the brain of peptide amyloid -, which is derived from amyloid precursor protein, and microtubule - associate protein tau are now much better understood. But efforts to convert this insight into gains in Clinic have flounder. Although researchers have conducted more than 400 trials in people for potential treatments for Alzheimer's Disease, almost no drugs have been brought to market. And despite blame being placed on a variety of factors, one of the main sources of researchers concern is animal models that are used in initial stages of drug development. The proposal that amyloid - peptides aggregate into structures known as plaques, from which other features of Alzheimers Disease stem, became the leading hypothesis of condition in the 1990s. Ever since, removing these peptide deposits has been viewed as a promising therapeutic strategy. However, no animal MODEL of Alzheimer's Disease was available in which such experiments could be perform. This is because researchers could find no evidence of conditions in organisms other than humans, which hamper discovery and development of potential drugs. Then, in 1995, researchers made breakthrough creation of transgenic mice carrying single gene mutation associated with uncommon, inherited form of Alzheimers Disease, which is characterized by early onset, at around the age of 45. Know as PD - APP mice, these animals express high levels of mutant APP in their brains and develop many hallmarks of Alzheimer's Disease, including plaques and cognitive deficits. Researchers draw confidence from structural similarity between mouse plaques and those found in people. Subsequent models similarly focus on expression of mutant APP. In 2006, several research groups generated mice containing multiple gene mutations associated with familial Alzheimer's Disease. Mice accumulate amyloid - deposits faster than AD - APP mice, with plaques appearing in the brain after only around 2 months, compared with at least 6 months in single - mutation mice. Such models provide researchers with important insight into Alzheimer's Disease. They show, for instance, that mutations associated with Inherited Alzheimers Disease favour production of variant of amyloid - called amyloid -, which is two amino acids longer than usual form and aggregate more readily. Models also serve as crucial preclinical test beds for drugs. In 1999, experimental vaccine was able to clear amyloid - from the brains of PD - APP mice. Several monoclonal antibodies have since been shown to clear plaques in mouse models. But all have failed to provide benefit to people with Alzheimer's Disease in trials. Even in cases in which drugs clear plaques from the brain, participants do not show improvements in memory. While mouse models have provided astounding new insights into disease mechanisms, says Bruce Lamb, neuroscientist at Indiana University School of Medicine in Indianapolis, they do reflect the entire biology of disease.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Trapped YAP

Alzheimer's Disease is the leading cause of dementia, and as many as 5 million people in the United States live with the disease. It causes a range of symptoms that begin with memory loss and confusion before progressing to difficulties with orientation, thinking, and speech. There is currently no cure for Alzheimers, and the exact cause of the disease remains unclear. However, scientists have found sticky clumps of protein called beta - Amyloid in the brains of people who have died of disease. This protein has been a major target for research to date. So far, trials of drugs that target beta - Amyloid have been unsuccessful. Some scientists think that this is because treatments have started too late. They believe that the process leading to Alzheimer's Disease starts many years before diagnosis and that once people join clinical trials, it may be too late to help them. Early stages of disease, therefore, represent a critical window in which to intervene. Scientists may also have discovered what causes neurons to die SO early in the disease process, suggesting that a protein called YAP is responsible. Previous genetic studies have found a link between YAP and Alzheimer's Disease. Yap, which regulates neuronal death, was present in lower levels in people with MCI. Interestingly, researchers found missing YAP trapped inside clumps of beta - Amyloid deposits that have the most known association with Alzheimer's Disease. This finding may change how scientists think about Alzheimer's Disease. Popular opinion among scientists is that beta - Amyloid Protein is the first trigger for Alzheimer's Disease, leading to death of neurons. They call this Amyloid hypothesis. However, these new findings suggest that loss of YAP Protein, which happens before Amyloid build up in the brain, might actually be the main cause of neuronal death. This discovery might change Amyloid hypothesis, says senior author Hitoshi Okazawa.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Sources

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

logo

Plex.page is an Online Knowledge, where all the summaries are written by a machine. We aim to collect all the knowledge the World Wide Web has to offer.

Partners:
Nvidia inception logo

© All rights reserved
2021 made by Algoritmi Vision Inc.

If you believe that any of the summaries on our website lead to misinformation, don't hesitate to contact us. We will immediately review it and remove the summaries if necessary.

If your domain is listed as one of the sources on any summary, you can consider participating in the "Online Knowledge" program, if you want to proceed, please follow these instructions to apply.
However, if you still want us to remove all links leading to your domain from Plex.page and never use your website as a source, please follow these instructions.