We previously reported data from models of primary mitochondrial dysfunction that arose through mitochondrial DNA (mtDNA) transfer from AD patients to neuronal cell lines depleted of their endogenous mtDNA (ρ0 cells),1, 12, 13 and more recently simply from ρ0 cells themselves; these models exhibit changes in AD‐associated biologies including changes in Aβ, tau, and apolipoprotein E (APOE [gene]; apoE [protein]) levels.14, 15, 16. This evidence concerns the gene MAPT and Alzheimer disease.