https://www.statnews.com/2018/10/29/alzheimers-research-outsider-bucked-prevailing-theory/

This topic deserves an in-depth essay, but, essentially, the Amyloid-plaque hypothesis, which has been the foundation of Alzheimer’s research since the 1990’s is … probably simply wrong. It originates with a failed pharma initiative related to drug development and profiteering.

The drugs have failed, miserably (none have succeeded), but a variety of myths continue to dog research… not the least of which is the poor quality of the clinical criteria for AZ diagnosis.

This researcher bucked the mainline hypotheses in a fashion common in good science — he inverted it, wondering if beta-amyloid plaques might be playing a crucial role in the brain’s immune system… and, so far, he has been able to demonstrate significant evidence for this.

“Dating to the 1980s, the amyloid hypothesis holds that the disease is caused by sticky agglomerations, or plaques, of the peptide beta-amyloid, which destroy synapses and trigger the formation of neuron-killing “tau tangles.” Eliminating plaques was supposed to reverse the disease, or at least keep it from getting inexorably worse. It hasn’t. The reason, more and more scientists suspect, is that “a lot of the old paradigms, from the most cited papers in the field going back decades, are wrong,” said MGH’s Rudolph Tanzi, a leading expert on the genetics of Alzheimer’s.”

“In the mush from Alzheimer’s patients’ hippocampus, which is ravaged by the disease and contains lots of beta-amyloid, candida growth plummeted compared to its riot of reproduction in both healthy brains and beta-amyloid-free Alzheimer’s cerebellum. But when Moir added antibodies that sideline beta-amyloid, the candida grew in the hippocampus like the yeast in a good sourdough.”