TOR-dependent cerebrovascular aging in Alzheimer's disease.

Abstract

Increasing evidence suggests that vascular dysfunction, a universal feature of aging, mechanistically contributes to the onset and pathogenesis of neurological diseases of aging. It was recently discovered that attenuating activity of the mammalian/mechanistic target of rapamycin (mTOR) extends both life- and health-span in mice by delaying aging. Here we review current evidence for a critical role of mTOR in age-associated vascular dysfunction and discuss potential mechanisms by which this pathway may lead to cognitive decline in Alzheimer's disease.