Unfortunately this review does not really provide any detail on the author's ideas. He did however publish a review 10 years ago [0] (a link to a free copy can

Unfortunately this review does not really provide any detail on the author's ideas. He did however publish a review 10 years ago [0] (a link to a free copy can be found on Google Scholar). There he comprehensively addresses the limitations of the amyloid hypothesis, especially that amyloid is not sufficient to cause Alzheimer's, either in humans or mice. The arguments have not changed much in the past 10 years, even if there has been some very modest success in clinical trials that remove amyloid from the human brain. The question then, is why the amyloid hypothesis still remains popular among scientists and clinicians. The simplest reason is that it is currently the only way to mechanistically link the various genes whose mutation causes early onset Alzheimer's (APP and presenilin), i.e. that APP is the source of amyloid, and presenilin is needed to produce amyloid from APP. Both genetically inherited Alzheimer's and the more common form share too many pathological features to be considered entirely separate diseases. Until there is an alternate explanation to mechanistically link presenilin, APP, and indeed apoE4, the amyloid hypothesis will always have its supporters. [0] The case for rejecting the amyloid cascade hypothesis, Karl Herrup https://www.nature.com/articles/nn.4017 https://www.nature.com/articles/nn.4017