Who Funds Alzheimers And Related Dementias Research
The National Institutes of Health is made up of Institutes, Centers, and Officesthat conduct and fund research into all aspects of human health. The National Institute on Aging leads NIHs efforts in clinical, behavioral, and social research in Alzheimers and related dementias through efforts aimed at finding ways to treat and ultimately prevent the disorder. NIA collaborates closely with the National Institute of Neurological Disorders and Stroke , which manages a research portfolio targeting Alzheimers disease-related dementias.While some of this research takes place in NIH laboratories, the vast majority of NIH support is provided through a competitive grants process to institutions and small businesses across the country. Other federal agencies support a range of activities focused on public health and community programs.
New Alzheimer’s Treatment Hailed By Researchers
Early results in a new treatment for one of the most common forms of dementia have been “absolutely spectacular”, according to researchers.
Alzheimer’s may be caused when a type of protein sticks to brain cells, eventually killing them.
A team including University of Leicester scientists tackled the protein before it was deposited.
Professor Mark Carr said early tests had completely halted disease progression in mice.
While the exact cause of Alzheimer’s is unknown, a strong candidate is amyloid beta protein forming ‘plaques’, which damage the brain.
Previous treatments, which tried to remove these plaques, have often failed to live up to early promise.
But the team, which also includes University Medical Center Gottingen in Germany and the medical research charity LifeArc, targeted a form of the protein before it became attached.
Prof Carr said using a vaccine or antibody to block the protein had worked well.
“It was absolutely spectacular. It’s not been seen with any other therapeutic approach that has been tried with Alzheimer’s,” he said.
“While the science is currently still at an early stage, if these results were to be replicated in human clinical trials, then it could be transformative.
“It opens up the possibility to not only treat Alzheimer’s once symptoms are detected, but also to potentially vaccinate against the disease before symptoms appear,” he said.
Amyloid Hypothesis Fails To Find Treatments
Scientists had been hopeful that amyloid which has been the primary focus of Alzheimers treatment research for the past three decades would be the key to solving Alzheimers. The plaque builds up around neurons the cells responsible for sending and receiving signals from the brain eventually leading to impaired memory and thinking in patients.
However, the recent controversy around Biogens aducanumab, allegations of falsified research and a series of failed clinical trials over the years targeting amyloid have left some in the field demoralized.
Most recently, pharmaceutical company Roche announced in June that its amyloid targeting drug, crenezumab, failed to slow or prevent cognitive decline in people with a rare genetic mutation that causes early-onset Alzheimers disease. The phase 3 trial, which the National Institute on Aging supported, enrolled around 250 people.
The amyloid hypothesis has been taking a lot of hits lately, said Donna Wilcock, the assistant dean of biomedicine at the University of Kentucky. The drug trials keep coming through and for the most part, failing.
Experts expect diagnosis and treatment of the disease may have to consider multiple mechanisms.
“Its an all-hands-on-deck kind of situation with research to try to identify better diagnosis and treatment options,” Ramanan said.
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What The Results Say
The researchers found that when the amyloid-beta proteins made in the liver of the test mice combined with fats and traveled to the brain, they interfered with the proper functioning of the brains microscopic blood vessels, or capillaries.
This dysfunction in the blood-brain barrier led to the protein-fat complexes leaking from the blood into the brain, resulting in inflammation. This inflammation occurred in both the test group and the control group, but it started at a much younger age in the test group.
Unlike in the control group, this inflammation was also associated with marked degeneration in the brain cells of the mice in the test group when examined under a microscope. The scientists only rarely saw this neurodegeneration in the control mice, and it was usually at a much older age.
The team also assessed a marker of neurodegeneration and found it to be approximately two times greater in the test mice than in control mice of the same age.
So, it was unsurprising that during the test for cognitive function, the test mice performed approximately half as well as the control group at retention of learning.
These findings suggest explanations to long standing questions about the role of amyloid-beta in Alzheimers disease development.
Warren Harding, board chairman of Alzheimers WA, revealed to MNT the significance of the study results. He said:
Former Whsmith Ceo Kate Swann Announced As New Chair Of Alzheimers Research Uk
Former CEO of SSP Group and WHSmith Kate Swann has been announced as the new Chair of Alzheimers Research UK with the business leader vowing to help lead the search for cures for dementia after witnessing first-hand the devastation the condition causes. Kate will become a Trustee of the charity from 1 October 2022,
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Jelly Drops: An Exciting New Invention To Help Combat Dehydration In Dementia
Inspired by his grandmother, Lewis Hornby has invented bite-sized sweets known as Jelly Drops to help reduce dehydration in dementia.Alzheimers Society was delighted to partner with Lewis and the Jelly Drops team this year through our Accelerator programme. Together, we’re working on bringing their fantastic product to people living with dementia.
Negative Thinking Can Harm Your Brain And Increase Your Dementia Risk
A new study shows that repetitive negative thinking, a mechanism proposed to underlie several known psychological Alzheimer’s disease risk factors, is itself associated with cognitive decline as well as amyloid and tau deposition on PET scans. Jacob Hall, MD, Clinical Assistant Processor of Neurology, comments on the study’s findings.
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Advances In Alzheimer’s And Related Dementias Research
As the nations biomedical research agency, the National Institutes of Health supports research spanning from basic biology to drug development to clinical studies to evaluating public health outcomes. Within the past several decades, researchershave made great strides toward better understanding what causes Alzheimers and related dementias and discovering approaches that may prevent, diagnose, and treat them.Some highlights of these efforts include:
Researchers Have Identified A New Type Of Dementia
In May, an international team of researchers identified a brain disorder known as LATE. It has similar symptoms to Alzheimers disease but appears to be caused by the build up of the toxic protein TDP-43.
Our researchers were able to delve into this particular protein by studying human brain tissue through our initiative Brains for Dementia Research.
The finding will help us distinguish between different brain disorders and develop precise and personalised treatments.
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A New Strategy For Alzheimers Disease Treatment Targets Cell
A new strategy that targets cell-wide protein malfunction shows promise for Alzheimers disease and brain cancers, according to a study published in Nature Communications on Aug. 3. The strategy has been used to create novel biomarkers and therapeutics, with a Phase 2 clinical trial for use in Alzheimers disease already underway.
The scientists behind the study are part of an NIA-funded team at the Sloan Kettering Institute that studies how proteins take shape and interact with each other, as well as how this process can go awry in disease. Their research looks at how genetic mutations and environmental stressors can change how a cell behaves. When these changes add up, the proteins in a cell do not interact with each other as they should, leading to disease.
For a cell to be healthy, proteins need to take on the right shape and interact in specific ways. A class of molecules called chaperones helps the proteins form correctly. In diseases like cancer, Parkinsons, and Alzheimers, chaperones stop working normally and become poisonous, causing the proteins in the cell to take on the wrong shape and interact with each other in ways that can cause disease. In cancer, for example, the malfunctioning proteins allow the cell to grow and divide in an uncontrolled way. In Alzheimers, the malfunctioning proteins include those that are essential for memory and thinking.
Senior Covid Survivors Could Be 80% More Likely To Develop Alzheimers: Study
As pioneers in neuroscience, we believe defeating this disease will require multiple approaches and treatment options, and we look forward to continuing the discussion about the significance of these findings with the patient, scientific, and medical communities, he said.
News of the milestone study, known as Clarity AD, also rippled in the finance world Biogens stock soared around $73 to $270 upon the major announcement, Yahoo! Finance reported.
We think that lecanemab holds mega blockbuster potential, likely in the $6 to $8 billion range, Guggenheim Partners analyst Yatin Suneja wrote in a client memo on Wednesday.
Lecanemab represents a major rebound for Biogen after Aduhelm the companys previous try at an Alzheimers treatment failed when brought to market in 2021, the New York Times reported.
The new drugs intended, neurological purpose is to clear away plaques formed on the brain by an Alzheimers-connected protein called amyloid, thus reducing the diseases major effects.
Eisai representatives will present the Clarity AD study findings to the Clinical Trials on Alzheimers Congress in late November and will publish the research to a peer-reviewed medical journal.
Eisai believes these findings will create new horizons in the diagnosis and treatment of Alzheimers disease as well as further activate innovation for new treatment options, company CEO Haruo Naito said.
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Seven Recent Papers Amplify Advances In Alzheimers Research
New findings from big-data and open-science research are revealing clues about the molecular mechanisms of Alzheimers disease and new ways to discover potential therapeutic targets and biomarkers. These new discoveries were made by six research teams participating in the Accelerating Medicines Partnership Alzheimers Disease program. AMP AD was established in 2014 as an NIH-led partnership among government, pharmaceutical industry, and nonprofit organizations that aims to transform the way we study the complex nature of Alzheimers disease.
AMP AD uses an open-science research model that makes all data and methods rapidly available to the research community at large through the data sharing infrastructure, the AD Knowledge Portal. Since the Portals launch in 2015, more than 3,000 researchers world wide from the academic, biotech, and pharmaceutical industry sectors have used the data resources for research on Alzheimers and related dementias.
Alzheimers is a complex disease, and as it slowly develops, many normal biological processes in the brain and the body go awry, from inflammation, to blood vessels damage and neuronal death. Seven recent AMP AD reports showcase research advances related to the discovery of new drug candidate targets, identification of molecular subtypes of the disease, and new potential biomarkers that can serve as the basis for a precision medicine approach to therapy development.
References:
The New Treatments For Ad
Alzheimers cure breakthrough studies and potential treatments have shown some promising results.
Dissolving the plaques: Most of the current focus on the management of AD has been targeting the protein plaques known as amyloid. These plaques are a classic feature of the disorder and often deposit early in the brain. Individuals who develop these plaques in the brain are more likely to develop symptoms of AD than those without plaques. Hence, several drugs have been developed that prevent the formation or clumping of these amyloid plaques. The monoclonal antibodies are very similar to the naturally occurring antibodies in the blood circulation, but they have only one target: amyloid beta. Unfortunately, amyloid is not found in all patients with AD and why this happens is not known. It is believed that close to 30%-35% of AD patients with mild to moderate disease may not have brain amyloid and, hence, cannot benefit from this treatment.
Currently, Aducanumab is only approved for use in select patients with mild cognitive impairment or early Alzheimers disease. Before the treatment can be administered, all individuals with AD must undergo a PET scan to determine if they have amyloid plaques.
Several other monoclonal antibodies have also been developed by different drug manufacturers and they also target amyloid in the brain. All these agents are currently being evaluated in clinical trials.
To be eligible for Aducanumab treatment, one has to meet the following criteria:
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Alzheimers Disease Causes Major Metabolic Changes In The Brain
Concept of memory loss and dementia disease and losing brain function memories as an alzheimers health symbol. Credit: Shutterstock
A collaboration between Weill Cornell Medicine scientists and other leaders in Alzheimers disease research has revealed widespread metabolic changes in the brains of individuals with Alzheimers disease. The findings could lead to the development of new treatments aimed at ameliorating the metabolic effects of the disease.
For the study, published July 13 in Alzheimers and Dementia, the investigators compared the levels of about 670 metabolites in postmortem human brain tissue samples obtained from people with Alzheimers disease and from those who did not have the condition. These metabolites are small molecules produced during key metabolic processes in the brain, such as producing energy for brain cells or processing fats essential for efficient transmission of information in the brain. Levels of more than half of the metabolites were altered in individuals diagnosed with Alzheimers. The team linked the metabolic changes with memory loss and the characteristic build-up of protein tangles in the brains of individuals with Alzheimers disease. In addition, the investigation revealed a new connection between cellular osmotic regulation and the disease.
This is a potential new mechanism in Alzheimers disease, he said.
When It’s Not Alzheimer’s: The Differential Diagnosis Of Frontotemporal Lobar Degeneration
The article is part of an ongoing series exploring the multiple differential diagnoses of Alzheimer’s disease. Frontotemporal lobar degeneration is estimated to cause up to 10% of dementia cases, and is often mistaken for Alzheimers. Dr. Sharon Sha, clinical assistant professor of neurology and neurological sciences, is interviewed about the differences.
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Study Shows Lecanemab Drug Slows Down Cognition Decline By 27% Compared To Placebo
Biogen Inc. headquarters are shown March 11, 2020, in Cambridge, Mass. Shares of Biogen and other drugmakers researching Alzheimers disease soared early Wednesday, Sept. 28, 2022, after Japans Eisai Co. said its potential treatment appeared to slow the fatal diseases progress in a late-stage study. Eisai announced results late Tuesday from a global study of nearly 1,800 people with early-stage Alzheimers.
Steven Senne, Associated Press
After an 18-month trial, pharmaceutical companies Biogen and Eisai report that results from a new study indicate a new clinical drug called lacanemab could be the next step in helping the Alzheimer’s community.
Dr. Susan Kohlhaas of Alzheimers Research UK told The Guardian that this is the first clinical trial in phase 3 to show a significant change in cognitive decline in a generation, and called it a historic moment for dementia research.
Whats the risk? Out of about 1,800 patients who participated in the trial, about 1 in 5 experienced side effects including brain swelling or bleeding, that have occurred with other medications similar to lecanemab.
The new medicine specifically targets amyloid plaques which are associated with Alzheimers disease, along with neurofibrillary tangles , per the National Institute of Aging.
Long-term effects are still being monitored.
Were not ready to deliver this at scale and we need to address that now, he said.
Talking About Mouseheimers And A Call For New Neuroscience Technologies
Michael Greicius, MD, MPH, professor of neurology & neurological sciences at Stanford, researches Alzheimers and has a bone to pick with media hype about Alzheimers research conducted in mice. What the mice have shouldnt be considered the same condition, he says, so hes termed it mouseheimers.
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Lecanemab The One Recent Exception
How will our findings affect drug development and clinical trials for Alzheimers disease? Until the recent trial with lecanemab, an antibody drug that reduces plaques, all the drug trials in Alzheimers disease have failed.
Some drugs were designed to reduce the levels of amyloid-beta 42, based on the rationale that if levels of the normal protein are reduced, patients will accumulate fewer plaques. Unfortunately, these drugs often made the patients condition worse.
Lecanemab was recently reported to have a small but significant effect in reducing cognitive decline. According to previous studies, this drug increases the levels of amyloid-beta 42 in the CSF. This is, again, in line with our hypothesis, namely that the increase of the normal amyloid protein can be beneficial.
We will know more when the results of the lecanemab trial are published. At the moment, all we have is a press release from the makers of the drug.
We think that it will be important for future trials to focus on the levels of amyloid-beta 42, and whether it is beneficial to increase and restore its levels to normal values instead of targeting it for removal. This could be achieved using proteins similar to amyloid-beta 42 so-called protein analogues but that clump together less than the natural ones.
This active protein replacement approach might become a promising new avenue of treatment for Alzheimers and other protein aggregation diseases, such as Parkinsons and motor neuron disease.
Alzheimers Disease Research Center
The Alzheimers Disease Research Center, part of NYU Langones Center for Cognitive Neurology, is one of 30 Alzheimers disease research centers in the United States supported by the National Institute on Aging . As an NIA-supported research facility, our aims are to advance current knowledge and understanding of brain aging and Alzheimers disease to expand the number of scientists working in the fields of aging and Alzheimers disease research and to work toward better treatment options and care for those living with memory impairment. Our ultimate goal is to share these findings with healthcare providers, researchers, and the general public to enhance the care of those affected by Alzheimers disease and related dementia.
Since 1973, our program has been at the forefront of research on memory problems attributed to normal aging, as well as a pioneer in the diagnosis, causes, and treatment of Alzheimers disease and related disorders. Our centers findings have added to the understanding of the effects of aging on the brain and the biology of Alzheimers disease. We have developed many of the scales and measures used throughout the world, tested new medications and novel procedures for brain imaging, and studied cerebrospinal fluid biomarkers.
A few of our most notable accomplishments include the following:
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