Kinda both. Increased presence of amyloid (a type of protein) plaques are common in patients with Alzheimer's disease, so it was hypothesized that these plaques contribute to alzheimers. The drugs mentioned specifically targeted these plaques (via monoclonal antibodies). These drugs didn't slow the progression of alzheimers in the patient population that was certain to get it. The drugs could have failed for two reasons I think: 1) the antibodies from the drugs were unable to break up the plaques (in which case the drug is the issue) or 2) the amyloid plaques themselves are actually being broken up by the drug...but the plaques may not really be a cause of alzheimers (in which case the hypothesis is the issue).