Beta-amyloid’s Key Role in Alzheimer’s Toxic Clumps and Need for Personalized Medicine Focus of Talk

Beta-amyloid’s Key Role in Alzheimer’s Toxic Clumps and Need for Personalized Medicine Focus of Talk
Increasing evidence places beta-amyloid aggregates at the center of the toxic protein clumps and neuroinflammation that drive Alzheimer’s, two experts in this disease said, and a personalized, combination treatment likely will be the best way of helping patients. These insights were shared at a recent Key Opinion Leader luncheon meeting, hosted by AC Immune in New York, that focused on the protein aggregates associated with Alzheimer’s and other neurodegenerative diseases, and possible future therapies or therapy approaches. Presentations given included those by Michael Weiner, MD, a professor of Radiology and Biomedical Imaging, Medicine, Psychiatry, and Neurology at University of California San Francisco School of Medicine and John Trojanowski, MD, a professor of Geriatric Medicine and Gerontology at the Perelman School of Medicine, University of Pennsylvania. Weiner, an expert in brain imaging and biomarkers to diagnose and monitor treatment response in neurodegenerative diseases, reviewed what is known about the role of beta-amyloid aggregates in the brain, which are — with  tau protein tangles — a hallmark of  Alzheimer’s disease. He said that increasing data support beta-amyloid aggregates as the most toxic aggregates in Alzheimer’s, and that their presence induces several events likely involved in the formation of tau protein clumps and neuroinflammation. Weiner emphasized that potential therapies against tau proteins curr
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    Twenty years ago it was published in Proc. Nat. Acad. Sci. USA. that amyloid-beta oligomers, i.e. soluble aggregates were the cytotoxic agents responsible for Alzheimer’s damage. Shortly after, it was shown that some natural immunoglobulins were protective against AD effect in transgenic animal models. Biogen has two monoclonal antibodies that protect against cyotoxic amyloid-beta. The amyloid-beta vaccines failed, because as designed they were supposed to fail. Perhaps it is long overdue to accept that the whole amyloid beta situation has been a tragicomedy of errors, rather than announcing “new discoveries” that are actually quite old rediscoveries.

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