Solanezumab and the amyloid hypothesis for Alzheimer’s disease

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Solanezumab’s failure is a wake-up call to look elsewhere for an answer to dementia

Is the amyloid cascade hypothesis of Alzheimer’s disease too big to fail? 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. 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.