What I find puzzling if the plaques are a link in the chain (as opposed to a symptom), isn't so much that beta-amyloid drugs stop short of outright resolving the symptoms, but that they don't seem to affect the progress of the disease.

To continue with your example, if beta-amyloid was a major source of inflammation, and inflammation caused the damage, it'd seem reasonable to expect that removing the plaques would result in slowed cognitive decline.

Strangely, this does not seem to happen in clinical trials.