Scientists may have overlooked a hidden Alzheimer's culprit for decades — SkimNews
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- Jevgenij Raskatov published a commentary in ChemBioChem arguing that P3, a peptide long assumed harmless, forms amyloid deposits faster than amyloid beta and may itself be neurotoxic, challenging decades of Alzheimer's research.
- Raskatov's UC Santa Cruz lab produced three major studies over five years showing P3 can aggregate, and an independent UK research group has since confirmed and extended the findings.
- Raskatov identified at least four peer-reviewed papers citing his team's research as evidence that P3 was inert — claims he called 'exactly the opposite of what we have actually shown.'
- Raskatov proposed renaming P3 to 'Amyloid α' (Aα) to reflect its overlooked aggregating abilities; the peptide forms when Amyloid Precursor Protein is first cut by α-secretase rather than β-secretase.
- UCLA emeritus neurology professor David Teplow said the reevaluation has 'far-reaching consequences for both basic science and clinical research' into Alzheimer's disease.
- Of more than 400 clinical trials for Alzheimer's drugs, most targeted amyloid beta; recently approved antibody therapies Lecanemab and Donanemab offer only modest benefits while carrying risks of brain hemorrhages and strokes.
Why it matters: More than 400 clinical trials targeting amyloid beta have yielded mostly disappointing results; Lecanemab and Donanemab offer only modest benefits while risking brain hemorrhages and strokes. UCLA's David Teplow now calls Raskatov's P3 evidence 'far-reaching consequences' for Alzheimer's drug development.
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