Solanezumab and the amyloid hypothesis for Alzheimer's disease.

David G Le Couteur, Sally Hunter, Carol Brayne

OAI: oai:www.repository.cam.ac.uk:1810/283306 • DOI: 10.17863/CAM.30674

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.

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