A drug that was seen as a major test of the leading theory behind Alzheimer’s disease has failed in a large trial of people with mild dementia. Critics of the ‘amyloid hypothesis’, which posits that the disease is triggered by a build-up of amyloid protein in the brain, have seized on the results as evidence of its weakness. But the jury is still out on whether the theory will eventually yield a treatment.
Proponents of the theory note that the particular way in which solanezumab, the drug involved in the trial, works could have led to the failure, rather than a flaw in the hypothesis itself. And many trials are ongoing to test whether solanezumab — or others that target amyloid — could work in people at risk of the disease who have not yet shown symptoms, or even in people with Alzheimer’s, despite the latest negative result.
“I’m extremely disappointed for patients, but this, for me, doesn’t change the way I think about the amyloid hypothesis,” says Reisa Sperling, a neurologist at the Brigham and Women’s Hospital in Boston, Massachusetts. She is leading one of several ongoing ‘prevention’ trials that is testing solanezumab, and other drugs that aim to reduce the build-up of amyloid ‘plaques’, in people at risk of developing Alzheimer’s.
Blood protein
Solanezumab is an antibody that mops up amyloid proteins from the blood and cerebrospinal fluid. The proteins can go on to form plaques in the brain. Eli Lilly, the company that developed solanezumab, announced on 23 November that it would abandon the drug as a treatment for patients with mild dementia. The outcome adds to a long list of promising Alzheimer’s drugs that have flopped in the clinic, many of which, like solanezumab, targeted amyloid… Read More>>
Source: Nature
