Human tau pathology is associated with lonely, nontraveling slow waves linked to memory impairment.

Memory markedly declines with age, exaggerated in those with Alzheimer's disease, yet the mechanisms are still not resolved. Here we show that frontal lobe tau pathology in humans is associated with impaired en masse unity and cortical traveling propagation of nonrapid eye movement slow waves, linked to impaired memory retention. We elucidate these findings using positron-emission tomography tau brain imaging, and then replicate and extend them using Alzheimer's disease pathology markers derived from cerebrospinal fluid in an independent clinical cohort. Thus, tau-associated memory deficits are not wholly direct but indirectly linked to consequential 'lonely', nontraveling slow-wave events.