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Drugs that target beta-amyloid, the molecule widely considered the cause ofย Alzheimerโs disease, make neurons function worse โ at least in mice โ explaining why anti-amyloid compounds have failed to improve memory or cognition inย clinical trials.
For nearly a quarter-century, the leading explanationย ofย Alzheimerโs disease has been that a protein called beta-amyloid (written ฮฒ-amyloid)ย is deposited around brain neurons, forming sticky โplaquesโ that eventually kill cells,ย destroy synapses, erase memory, and cripple cognition. The amyloid hypothesis has beenย so dominant โ virtually every pharmaceutical and biotech company trying to develop anย Alzheimerโs drug is on the amyloid warpath โ that scientists pursuing other explanationsย have warned that โThe Church of the Holy Amyloidโ has choked off research on competing ideas.ย The real tragedy has been the repeated failures of experimentalย compounds targeting amyloid: They often clear away amyloid but donโtย help symptoms.
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In a new study, scientists injected a form of the Pfizer-J&J anti-amyloid antibody, orย a similar one from Novartis, into mice whose brains wereย riddled with ฮฒ-amyloid plaques. The Pfizer-J&J compound sopped up amyloid in the mice; Novartisโs had less effect. But the shocker was that both antibodies madeย neurons become hyperactive, reported Marc Busche of Technical University of Munich and colleagues (including two from Novartis) in Nature Neuroscience.
Read full, original post:ย Top Alzheimer’s approach makes (mice) brains worse
