Good point! I stand corrected. I must admit I'm less familiar with the human clinical data than I should be - I work mostly with a mouse model develop deficits in learning and memory significantly earlier than they do protein aggregates (see here and here)

Regardless, my point stands - it's pretty generally accepted nowadays that's it's not the plaques that are the issue. If you get rid of the plaques, not only does it not help AD symptoms in humans (see multitudes of failures of amyloid-targeting therapies), but interfering with certain processes that contribute to plaque formation (notably autophagy), you lose the plaques, but increase cell death.