An experimental Alzheimer’s drug that had previously appeared to show promise in slowing the deterioration of thinking and memory has failed in a large Eli Lilly clinical trial, dealing a significant disappointment to patients hoping for a treatment that would alleviate their symptoms.

The failure of the drug, solanezumab, underscores the difficulty of treating patients who have reached the point of showing even mild dementia, and supports the idea that by that time the damage in their brains may already be too extensive. And because the drug attacked the amyloid plaques that are the hallmark of Alzheimer’s, the trial results renew questions about a leading theory of the disease, which contends that it is largely caused by amyloid buildup.

http://www.nytimes.com/2016/11/23/he...rial.html?_r=0

This result was disappointing, although not surprising. It's important for PWP because, conceptually, solanezumab (a monoclonal antibody) works the same way that the anti A-Syn vaccines work. It just targets a different protein, Amyloid. There are probably a lot of reasons why the drug failed (tau may be the appropriate target, not amyloid; the patients may have been too far progressed, etc). However, we need to keep in mind that when we see early trial results from Prothena, AffiRis and Proclara that show reduction of A-syn. You still have to prove that reducing cerebral fluid levels of the protein will actually lead to improvement in symptoms and slowing or stopping the progression. We still have a long way to go.