Solanezumab and the amyloid hypothesis for Alzheimer's disease.
Accepted version
Peer-reviewed
Repository URI
Repository DOI
Change log
Authors
Le Couteur, David G
Hunter, Sally https://orcid.org/0000-0002-8063-6556
Brayne, Carol https://orcid.org/0000-0001-5307-663X
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
1756-1833
Volume Title
355
Publisher
BMJ