So far, much effort has been devoted to the clearance of Aβ plaques as a strategy to defeat or delay the onset of dementia of Alzheimer’s, explaining why the Amyloid Hypothesis, which posits that it is AB plaques, themselves, that are the cause of Alzheimer’s dementia, has persisted without an eye toward the thought of interfering in the driving power of neuroinflammation, i.e., IL-1β, the driver of the cardinal features of not only Alzheimer’s but of Parkinson’s. This evidence concerns the gene IL1B and Parkinson disease.