[ABetaMale]

That's a natural a priori hypothesis but there's extremely strong evidence that amyloid is causally upstream.

For example, mutations in the enzymes or proteins involved in the production of amyloid-β (APP, PSEN1, and PSEN2), which structural analysis show have the direct effect of producing either more total amyloid-β, or more of amyloid-β 42 (the specific peptide implicated in Alzheimer's), deterministically cause Alzheimer's. That puts amyloid-β causally upstream at least in those cases, the so-called autosomal dominant variety, which are ~1% of Alzheimer's cases.

The remaining ~99% of cases are less straightforward to interpret, but the disease looks essentially the same as the ~1% of cases described above: first amyloid-β builds up in the default mode network, then it spreads throughout the brain, eventually reaching the medial temporal region where primary age-related tauopathy (PART) is waiting, only then does the tau pathology spread, and neurodegeneration follows the tau pathology in lockstep. The way the amyloid-β and tau proteins misfold in autosomal dominant and sporadic Alzheimer's are the same, too, even though other tau pathologies have different tau folds. So basically, there's every reason to believe sporadic Alzheimer's is essentially the same disease as the one which we're basically certain is caused by amyloid-β.