Why Is Research on Amyloid-ß Failing to Give New Drugs for Alzheimer’s Disease?

Andrew Doig, Maria Del Castillo Frias, Olivia Berthoumieu, Bogdan Tarus, Jessica Nasica-Labouze, Fabio Sterpone, Phuong H Nguyen, Nigel M Hooper, Peter Faller, Philippe Derreumaux

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    The two hallmarks of Alzheimer’s disease (AD) are the presence of neurofibrillary tangles (NFT) made of aggregates of the hyperphosphorylated tau protein and of amyloid plaques composed of amyloid-β (Aβ) peptides, primarily Aβ1-40 and Aβ1-42. Targeting the production, aggregation and toxicity of Aβ with small molecule drugs or antibodies is an active area of AD research due to the general acceptance of the amyloid cascade hypothesis, but thus far all drugs targeting A have failed. From a review of the recent literature, and our own experience based on in vitro, in silico and in vivo studies, we present some reasons to explain this repetitive failure.
    Original languageEnglish
    Pages (from-to)1435-1437
    Number of pages3
    JournalACS Chemical Neuroscience
    Issue number7
    Early online date6 Jun 2017
    Publication statusPublished - 19 Jul 2017


    • amyloid-β
    • Alzheimer’s disease
    • in vitro and in vivo studies
    • Computer simulations
    • drugs


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