Setting The Federal Research Agenda
NIH takes a collaborative, methodical approach to reviewing progress, identifying gaps, and setting the future agenda for research into Alzheimers disease and related dementias. NIH funding in this area is guided by gaps and opportunities identified in researchsummits, which alternate yearly to focus on Alzheimers disease, Alzheimers disease-related dementias, or dementia care and services.Smaller, focused workshops are held more frequently on specific aspects of this research.
NIH outlines its Alzheimers research efforts in theNIH AD/ADRD Research Implementation Milestones, a research framework detailing specific steps and success criteria toward achieving the goals of theNational Plan to Address Alzheimer’s Disease. The milestones also showcase funding initiatives, accomplishments, and highlights of progress toward accomplishing the National Plan goals.
NIHs research progress is highlighted in the annualAlzheimers and related dementias professionaljudgment budget, which is submitted to Congress each year.
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:
Therapy Manipulates The Immune System To Slow Neurodegeneration Without Triggering Dangerous Inflammation In The Process
A new therapy prompts immune defense cells to swallow misshapen proteins, amyloid beta plaques and tau tangles, whose buildup is known to kill nearby brain cells as part of Alzheimers disease, a new study shows.
Led by researchers at NYU Grossman School of Medicine, the investigation showed that elderly monkeys had up to 59 percent fewer plaque deposits in their brains after treatment with CpG oligodeoxynucleotides , compared with untreated animals. These amyloid beta plaques are protein fragments that clump together and clog the junctions between nerve cells .
Brains of treated animals also had a drop in levels of toxic tau. This nerve fiber protein can destroy neighboring tissue when disease-related changes to its chemical structure cause it to catch on other cells.
Our findings illustrate that this therapy is an effective way of manipulating the immune system to slow neurodegeneration, says Akash Patel, MS, an assistant research scientist in the Center for Cognitive Neurology at NYU Langone Health.
The investigators say the treatment led to cognitive benefits as well. When presented with a series of puzzles, elderly monkeys given the drug performed similarly to young adult animals and much better than those in their age group that had remained untreated. The treated monkeys also learned new puzzle-solving skills faster than their untreated peers.
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Pilot Study Suggests Therapy Horses May Aid People With Dementia And Their Caregivers
The research team, led by Dolores Gallagher Thompson, PhD, and Nusha Askari, PhD, and Jacqueline Hartman at the Stanford Red Barn Leadership Program, found that supervised activities, such as observing herd behavior, grooming horses and leading horses with a lead and halter, helped participants recognize and use non-verbal forms of communication.
The Devastation Of Alzheimers Disease
With all this said, we are extremely aware of the gradual and cumulative devastation that Alzheimers disease causes, as patients lose their memory and cognitive functioning over time. In late-stage disease, people can no longer hold a conversation or respond to their environment. On average, a person with Alzheimers disease lives four to eight years after diagnosis, but some patients can live up to 20 years with the disease.
The need for treatments is urgent: right now, more than 6 million Americans are living with Alzheimers disease and this number is expected to grow as the population ages. Alzheimer’s is the sixth leading cause of death in the United States.
Although the Aduhelm data are complicated with respect to its clinical benefits, FDA has determined that there is substantial evidence that Aduhelm reduces amyloid beta plaques in the brain and that the reduction in these plaques is reasonably likely to predict important benefits to patients. As a result of FDAs approval of Aduhelm, patients with Alzheimers disease have an important and critical new treatment to help combat this disease.
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Definition Of Associated Loci
A region of ±500kb was defined around each variant with a stage I P value below 1×105. These regions were then merged to define nonoverlapping regions. The region corresponding to the APOE locus was excluded. We then used the PLINK clumping procedure to define independent hits in each region. An iterative clumping procedure was applied to all variants with a stage I P value below 1×105, starting with the variant with the lowest P value . Variants with a stage I P value below 1×105, located within 500kb of this index variant and in LD with the index variant were assigned to the index variants clump. The clumping procedure was then applied until all the variants had been clumped. LD in the EADB-TOPMed dataset was computed using high-quality imputed genotypes.
Success Of Experimental Alzheimers Drug Hailed As Historic Moment
Study shows cognition in early-stage patients on lecanemab declines by 27% less than those on placebo
An experimental drug has slowed the rate of decline in memory and thinking in people with early Alzheimers disease in what is being described as a historic moment for dementia treatment.
The cognition of Alzheimers patients given the drug, developed by Eisai and Biogen, declined by 27% less than those on a placebo treatment after 18 months. This is a modest change in clinical outcome but it is the first time any drug has been clearly shown to alter the diseases trajectory.
This is a historic moment for dementia research, as this is the first phase 3 trial of an Alzheimers drug in a generation to successfully slow cognitive decline, said Dr Susan Kohlhaas, the director of research at Alzheimers Research UK. Many people feel Alzheimers is an inevitable part of ageing. This spells it out: if you intervene early you can make an impact on how people progress.
In the study, which enrolled roughly 1,800 patients with early stage Alzheimers, patients were given twice-weekly infusions of the drug, called lecanemab. It was also shown to reduce toxic plaques in the brain and slow patients memory decline and ability to perform day-to-day tasks.
About a fifth of patients experienced side-effects, including brain swelling or brain bleeding visible on PET scans, with about 3% of those patients experiencing symptomatic side-effects.
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Love Island Star And Olympian Greg Oshea To Run London Marathon For Alzheimers Research Uk In Memory Of Grandmother
Love Island favourite and former international rugby player Greg OShea will run the TCS London Marathon in October to support the work of Alzheimers Research UK. Greg, who won the hit reality show in 2019, will be running in memory of his grandmother, Monica Ho, who passed away with dementia while he was in the
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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Thwarting A Protein Reverses Brain Decline In Aged Mice
Impeding VCAM1, a protein that tethers circulating immune cells to blood vessel walls, enabled old mice to perform as well on memory and learning tests as young mice, a Stanford study found. Senior author Tony Wyss-Coray, professor of neurology and neurological sciences, co-director of the Stanford Alzheimers Disease Research Center, is quoted in this piece.
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.
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Can Major Surgery Increase Risk For Alzheimers Disease
Dr. Greicius and colleagues in anesthesia , have shown that p-tau181, a blood-based Alzheimers biomarker, increases significantly during surgery and rises to levels typically seen in patients with Alzheimers disease. The p-tau181 levels slowly decline after surgery but remain elevated in some patients for at least two days after surgery. The study paves the way for future work that will try to link molecular changes induced by surgery to the longer term post-operative decline that occurs in some surgical patients.
Expression In Various Cell Types
The expression of genes was assigned to specific cell classes of the adult brain, as described previously. Briefly, middle temporal gyrus single-nucleus transcriptomes from the Allen Brain Atlas dataset were used to annotate and select six main cell classes using Seurat 3.1.1 : glutamatergic neurons, GABAergic neurons, astrocytes, oligodendrocytes, microglia and endothelial cells. Enrichment analyses were performed by using the mean gene expression per nucleus for each cell type relative to the total expression summed across cell types as a quantitative covariate in a MAGMA gene property analysis.
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Focusing On Cause Not Effect Could Unblock Alzheimers Research Scientists Hope
Alzheimer identified deposits of protein that had accumulated in the brain of a patient who died from dementia. In the years since, research has heavily focussed on the fragments of protein, known as amyloid-beta, that form these toxic plaques. The theory goes: if we can clear these plaques, then we can stop the brain cells from dying.
Despite billions of euros invested in research, there is little to show for patients. Current treatments can only mask the symptoms for a while, but there is still no way to stop or even slow the progress of the underlying disease.
One of the main difficulties in finding an effective treatment is that it is hard to recreate Alzheimers disease in the lab. No other animal develops the condition, and studies often rely on genetically-modified mice as models of the disease.
We have hundreds of drugs that work nicely and improve the outcome of mice when they have Alzheimers disease-like symptoms. So there is a complete translational block from preclinical studies to the clinic , said Professor Jari Koistinaho from the University of Eastern Finland.
The fundamental challenge is that we still do not know how Alzheimers disease is triggered. The first stages could begin decades before symptoms appear, making it extremely difficult to understand how those first moments influence everything that follows. Figuring this out could help to create models that more closely represent the disease we see in people.
Turning the clock back
New Therapeutics In Alzheimer’s Disease
DPUK’s New Therapeutics in Alzheimer’s Disease study is looking to detect subtle markers of Alzheimer’s disease that are visible in the brain before symptoms appear. These indicators will be used to test whether experimental treatments are successful in delaying, or even preventing, the progression of the disease.
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Genetic Overlap With Other Neurodegenerative Diseases
We tested the association of the lead variants within our new loci with the risk of developing other neurodegenerative diseases or AD-related disorders . We also performed more precise colocalization analyses for five loci known to be associated with Parkinsons disease , types of frontotemporal dementia and amyotrophic lateral sclerosis . The IDUA signal for Parkinsons disease was independent of the signal in ADD 3=99.9%), but we were not able to determine whether the CTSB signals colocalized. The TMEM106B and GRN signals in frontotemporal lobar degeneration with TAR DNA-binding protein inclusions probably share causal variants with ADD . Lastly, we were not able to determine whether the TNIP1 signals colocalized for ADD and amyotrophic lateral sclerosis.
New Findings In Down Syndrome And Alzheimers Disease Research
Contributed by Alessandra C. Martini, PhD, Associate Project Scientist at UCI MIND
Researchers have discovered that the majority of people with Down syndrome will have the pathology of Alzheimers disease amyloid plaques and neurofibrillary tangles in their brains by 40 years of age.
In this new study, conducted with colleagues at the University of Kentucky, we used autopsy tissue donated by research participants to analyze the role of microglia in the development of Alzheimers disease in people with Down syndrome across different ages and disease stages.
What we found is that people with Down syndrome, and especially those with Alzheimers disease pathology, have a particular kind of microglia cell that is more damaged compared to people without Down syndrome. This suggests that individuals with Down syndrome have a different immune response in their brains that may impact how they respond to Alzheimer disease pathology. This will be an important consideration for future studies and drug development for people with Down syndrome and Alzheimers disease.
Alessandra Martini, PhD
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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.
What Is A Professional Judgment Budget
Each year NIH submits a professional judgment budget that estimates the additional funding needed to advance NIH-supported research into the treatment and prevention of Alzheimers disease and related dementias. The report also summarizes progress and promising research opportunities. Only two other areas of biomedical research cancer and HIV/AIDS follow a similar process designed to accelerate research discovery. This approach is often referred to as a bypass budget because of its direct transmission to the President and then to Congress without modification through the traditional federal budget process.
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Why Should You Donate Your Brain To Science
Ever wonder what happens after you donate your brain to science? If you have a disease or disorder like Alzheimers, Parkinsons, autism, traumatic brain injuries, depression, it can be used to help researchers better understand the condition and potentially lead to new treatments. But scientists also need to study the brains of people unaffected by any type of disease. Science Friday radio broadcast hosted by Ira Flatow, Why Should You Donate your Brain to Science?
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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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.
New Study Points To Targetable Protective Factor In Alzheimer’s Disease
From the NIH Directors Blog by Dr. Francis Collins
If youve spent time with individuals affected with Alzheimers disease , you might have noticed that some people lose their memory and other cognitive skills more slowly than others. Why is that? New findings indicate that at least part of the answer may lie in differences in their immune responses.
Researchers have now found that slower loss of cognitive skills in people with AD correlates with higher levels of a protein that helps immune cells clear plaque-like cellular debris from the brain . The efficiency of this clean-up process in the brain can be measured via fragments of the protein that shed into the cerebrospinal fluid . This suggests that the protein, called TREM2, and the immune system as a whole, may be promising targets to help fight Alzheimers disease.
The findings come from an international research team led by Michael Ewers, Institute for Stroke and Dementia Research, Ludwig-Maximilians-Universität München, Germany, and Christian Haass, Ludwig-Maximilians-Universität München, Germany, and German Center for Neurodegenerative Diseases. The researchers got interested in TREM2 following the discovery several years ago that people carrying rare genetic variants for the protein were two to three times more likely to develop AD late in life.
This research was supported in part by NIA grants R01AG044546, P01AG003991, RF1AG053303, R01AG058501, U01AG058922, U01AG024904, AG047644, R01AG051812, and R01AG054672.
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