Researchers this week say their work should upturn the conventional narrative of how Alzheimer’s disease happens. They argue the progression of Alzheimer’s is driven by a very specific form of two proteins that play a crucial role in the disease, and these forms should be considered prions—potentially infectious proteins that self-replicate by turning their brethren into a misfolded version of themselves. To put it simply, people with Alzheimer’s disease have brains that are filled with rigid, clumped-together deposits of the proteins amyloid beta and tau, called plaques and tangles, respectively. It’s long been assumed that if we can stop these...