Thinking speculatively, what happens if we prevent the whole plaque formation problem - which really does seem to be an issue of humans living well past our paleolithic warranty period - by knocking out the amyloid precursor protein altogether in our descendants? Knockout mice have been around for a while; what's their phenotype like? Not great. They demonstrate:
This does not sound like an opportunity for enhancement. Original paper here.
decreased neuromuscular performance
reactive gliosis in the hippocampus & cortex (later in adult life)
reduced synaptic plasticity
loss of synaptic immunoreactivity for:
defects in the corpus callosum
The knockout mice also do much worse in a cerebral ischemia paradigm, related to the reactive gliosis seen in the list. If APP is involved with resistance to or recovery from infarct, this is consistent with the observed increase in Alzheimers and amyloid plaque formation in humans after cerebral infarcts.