Open AccessWhy Is Research on Amyloid-β Failing to Give New Drugs for Alzheimer’s Disease?
Author(s) -
Andrew J. Doig,
Maria P. del CastilloFrias,
Olivia Berthoumieu,
Bogdan Tarus,
Jessica Nasica-Labouze,
Fabio Sterpone,
Phuong H. Nguyen,
Nigel M. Hooper,
Peter Faller,
Philippe Derreumaux
Publication year - 2017
Publication title -
acs chemical neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.158
H-Index - 69
ISSN - 1948-7193
DOI - 10.1021/acschemneuro.7b00188
Subject(s) - amyloid (mycology) , in vivo , biochemistry of alzheimer's disease , disease , alzheimer's disease , in silico , neuroscience , amyloid β , pharmacology , in vitro , tau protein , medicine , amyloid precursor protein , chemistry , biology , pathology , biochemistry , microbiology and biotechnology , gene
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 Aβ 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.
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