John Hardy, a professor of neurology at University College London, developed his hypothesis on the cause of Alzheimer’s disease (AD) in 1992. This explained the three key features of AD: the build-up of sticky plaques in the brain called amyloids, tangles of amyloids with another protein (called tau) and the death of brain cells owing to the reaction between the two protein types causing neuronal death.
This theory clearly highlighted the way in which an effective AD drug might work. And 30 years later, in 2022, clinical trial results on a drug called Lecanemab validated professor Hardy’s theory by showing, for the first time, that a drug can both reduce amyloid plaques and significantly slow cognitive decline in early AD patients.
Lecanemab was developed by biotechnology companies Biogen and Eisai. Their phase-III (final-stage) clinical trial on 1,795 patients with early AD showed that cognitive decline over 18 months was 27% slower for patients on Lecanemab compared
