Both drugs target beta amyloid plaque, the sticky gunk that accumulates in the brains of people with the disease.
These failures have revived doubts over the long-held theory that beta amyloid is crucial in causing the disease. The hypothesis has been criticised in the past, particularly after post-mortems showed the presence of amyloid plaques in people who didn’t develop Alzheimer’s.
Getting real good at what seems like eliminating the wrong thing. This is how science works. That theory should be shelved, and others reinvigorated.