Consensus among Alzheimer’s researchers about the origins of the disease is growing. Most, including members of Cure Alzheimer’s Fund Research Consortium, agree that a combination of factors, beginning with the excessive build-up of the peptide Abeta42 triggering the development of tau tangles, nerve cell death, and inflammation are all required for Alzheimer’s pathology.
A new study by David Holtzman of Cure Alzheimer’s Fund’s Research Consortium published by the journal “Science Translational Medicine” brings sharp new focus on the direct relationship between the accumulation of Abeta in the brain and notorious sleep problems associated with Alzheimer's disease. This NIH-funded study (also supported by Ellison Medical Foundation) was made possible by early pilot studies initiated by the Cure Alzheimer's Fund --- another great example of leveraging innovative research ideas into substantially funded, high impact projects.
A study just published in the New England Journal of Medicine points to the value of conducting a new series of Alzheimer's prevention studies, suggests Cure Alzheimer's Consortium member Sam Gandy in an accompanying NEJM editorial. The study, led by Washington University's Randall J. Bateman, found that patients with a more genetic-oriented form of Alzheimer's experience a rise in beta-amyloid (Aβ) up to 25 years before symptoms begin -- and an increased level of tau protein up to 15 years before symptoms.
On Friday, August 24, Eli Lilly announced that their beta-amyloid immunotherapy (solanezumab) failed to meet its primary clinical endpoints for Alzheimer's disease. This disappointment follows the recent failure of another promising beta-amyloid immunotherapy, bapineuzumab from Pfizer/Johnson and Johnson-Jannsen/Elan. Both drugs failed in Phase 3 clinical trials, where they were being tested for their actual effect on Alzheimer's patients.
Genes are the specific DNA blueprints for life, and all genes play roles that are essential for health. But some can carry DNA variants that influence risk for disease, either by increasing or decreasing susceptibility. If a variation in a gene is very rare, it’s called a mutation. The mutation may cause disease, increase risk for a disease, protect against a disease, or have no impact on health at all.
Alzheimer’s research for many years has been dominated by a focus on Abeta “plaques,” a focus that largely has overlooked the other infamous hallmark of the disease—the tau-based neurofibrillary “tangles.” The research world recently has broadened its scope to include significant research into tau.
Cure Alzheimer’s Fund Research Consortium member David Holtzman’s latest paper has been published in the Journal of Neuroscience, addressing how Alzheimer’s plaques affect brain networks.
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