Although mitochondrial abnormality has been observed in AD patients and in transgenic mice expressing P301L mutated tau (the latter is only seen in patients of FTDP-17 but not AD), and the N-terminal truncated tau proteins were detected in mitochondria [18-23], our current study provides the first direct evidence showing that intracellular accumulation of wild type full-length tau inhibits mitophagy, which reveal a novel mechanism underlying tau-induced neurodegeneration in sporadic AD patients. This evidence concerns the gene MAPT and Alzheimer disease.