The present hypotheses may also have major implications formedical research and ultimately for treatment: (1) the pathways that allow thereversal of hyperphosphorylated tau in starving rats will hold key clues toreversing or preventing AD (2) the close evolutionary association with diabetesmellitus and other thrifty disorders should influence researchers to focus onpathocomparative analyses (3) theorists now have a reason to reconcile the vastliterature on thrifty genes, deprivation syndromes and phenotypic plasticity withthe literature on the pathophysiology of AD. The gene discussed is MAPT; the disease is Alzheimer disease.