MAPT and Alzheimer disease: These findings confirm and further extend our previous studies reporting a noxious effect exerted by NH2htau fragment on the normal physiology of neuronal mitochondria in AD [52, 53], demonstrating that its 12A12mAb-mediated in vivo clearance could be also exploited to mitigate the visual deficits associated with mitochondrial dysfunction due to the retinal accumulation of pathogenetic tau species [63, 108].