Exactly right...also note this well known contradiction (AFAIK) has been casually stepped OVER(overlooked) for decades by the FDA (no mention/research or public explanation for how it is possible) as they lead-drove decades of searching for "THE" solution to AD Cause. ...in fact it is not mentioned or evaluated by FDA/NIH..., even in passing....DECADES AND BILLIONS$$$ are big nums, in my book.
An incomplete analogy: Two fireplaces are filled with kindling. One also has a blowtorch nearby and the other just a lit cigarette. Only one quickly turns into a roaring fire. Kindling is amyloid, the intense flame is a cluster of tau. Prevent the clustering of tau and less chance for AD. (the analogy breaks down because the amyloid may increase tau clustering in most people) . The man and his sister still developed AD but at a later age. AD is complicated and not controlled by a single gene in a one step pathway. Mutations help us understand but the story is still being written. Another member of the large Colombian cohort with the PSEN mutation predisposing AD (leading to early and intense amyloid deposition) had a mutation in her ApoE3. Her brain was filled with mutated amyloid that did not induce tau clusters. Amyloid removal coupled to tau regulation may be the route for the majority of us lacking favorable mutations.