A recent study I've seen suggests that all three might have a causal role to play. Going from memory, the research suggests that amyloid plaque is part of an immune response to pathogenic infections in the brain. So herpes or P. gingivalis infections might trigger the build up of the plaque. The other causal factor is that certain forms of these plaques have prion-like properties, in that they induce a malfolding that has increased toxicity.

Wouldn't it be incredible if multiple independent lines of inquiry converged into a single unified explanatory framework?