4 ms·

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

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).

jcranmer 7y ago
> 2) the amyloid plaques themselves are actually being broken up by the drug This is actually what several studies have shown--the amyloid plaques were being removed by the drugs, but the progression of Alzheimer's was not slowed or halted.
- hprotagonist 7y ago
  Different disease, but if you really want to be depressed: https://blogs.sciencemag.org/pipeline/archives/2017/05/18/now-this-is-a-drug-that-does-not-work https://blogs.sciencemag.org/pipeline/archives/2017/05/18/no...
n0rbwah 7y ago
> 1) the antibodies from the drugs were unable to break up the plaques (in which case the drug is the issue) Shouldn't it be possible to have a look at the patients brains to see if there's any difference in plaque formation in those that underwent treatment vs those who had the placebo.