MAPT and Alzheimer disease: In order to identify the plausible mechanistic interaction of truncated Aβ and NH2-tau peptides in impaired neuronal mitochondria, data on reciprocal coimmunoprecipitations on synaptic-enriched mitochondrial fractions suggest that an NH2-tau/ANT-1/Aβ/CypD complex exists within an authentic cellular context in AD but not in age-matched nondemented controls.