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Solanezumab and the amyloid hypothesis for Alzheimer's disease.

Accepted version
Peer-reviewed

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Type

Article

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Authors

Le Couteur, David G 

Abstract

Is the amyloid cascade hypothesis of Alzheimer’s disease too big to fail?1 It proposes that brain deposition of β amyloid protein is the critical early event in the pathogenesis of Alzheimer’s disease and has been the centrepiece of dementia research for decades.2 The hypothesis suggests that removing β amyloid will reverse or prevent the clinical expression of dementia. However, in all phase III clinical trials to date, treatments targeting β amyloid have failed to improve cognitive outcomes despite reducing brain β amyloid.

Description

Keywords

Alzheimer Disease, Amyloid beta-Peptides, Antibodies, Monoclonal, Humanized, Humans, Plaque, Amyloid, Treatment Failure

Journal Title

BMJ

Conference Name

Journal ISSN

0959-8146
1756-1833

Volume Title

355

Publisher

BMJ