There is a testable prediction in your article. Unfortunately, I don't think the mechanism is quite restricted enough. TFA says that repairing the BBB helps amyloid plaque clearance. Would the author of your blog post claim that as a win, or admit that the plaques are downstream of the problem, and that BBB integrity is closer to the root cause of the disease process?

The author of that blog post, for whom I am in an excellent position to speak, would point to the "sole intended mechanism" clause in the testable prediction. That is, if the therapeutic's developers do not claim any other intended pathway for clinical benefit from improved BBB integrity other than amyloid−β clearance, then it would count. If not, then it would not count, even if it's plausible or even likely that that's the main pathway by which the benefits are accruing.

However, because this is early preclinical research, it's not likely to reach a late-stage clinical trial within the 12-year window of the author's prediction. Furthermore, in every year there are about a dozen of these preclinical studies that go viral for some reason or other, often having little correlation with how promising the science is. I haven't had a chance to look into this one in detail, so this isn't a negative comment about it, but the base rate of this stuff panning out is low, even if it's good research.

The author of that article would also point out that the concept of "the root cause" isn't terribly well-defined, but that strong evidence points to amyloid pathology as the common entrypoint in all cases of Alzheimer's disease, even if multiple upstream factors (some possibly relating to the BBB) can feed into that, depending on the specific case. Similarly, calorie surplus causes obesity in nearly all cases, but the specific cause of calorie surplus may vary from person to person.

I can't guess what point you're trying to make with a long article that acknowledges the fraud in the beginning, and then rehashes the initial reasons for looking into the amyloid hypothesis. No one is claiming it was stupid to look into the amyloid hypothesis. They are complaining that it hasn't been the most promising theory in quite a long time, and it was fraudulently held as the most promising. Other theories, arguably more promising, are listed throughout your article.

A correction: the article does discuss other hypotheses, in pointing out that they can't account for crucial evidence, whereas there isn't any major evidence the amyloid hypothesis seems to have trouble accounting for, and it thus remains very strong.