The long years of failure in Alzheimer’s research, in which trial after trial of immunotherapies targeting amyloid-β produced no meaningful benefits in Alzheimer’s patients, has sown the seeds of change in the research community. In the past couple of years, promising human data for amyloid-β clearance has finally arrived, but the damage is done. The amyloid hypothesis for Alzheimer’s disease is now challenged, and alternative theories are thriving. One of particular note is built upon the point that generation of amyloid in the brain appears to be a defensive mechanism of the innate immune system, and thus its proponents see Alzheimer’s as the end result of persistent infection, such as by herpesviruses or the bacteria of lyme disease.
In this view of the world, Alzheimer’s is just another of the many unpleasant late consequences of a high disease burden sustained throughout life. We are, after all, far better off than our recent ancestors thanks to increased control over infectious disease. Chronic inflammation and other consequences of the burden of parasitism and infectious disease resulted in earlier frailty in later life and shortened life expectancy until the advent of widespread antibiotics and other,