mTOR drives cerebrovascular dysfunction and blood-brain barrier breakdown in a model of Alzheimers disease with cerebral amyloid angiopathy

Cerebral amyloid angiopathy (CAA) is characterized by the deposition of amyloid {beta} fibrils (A{beta}) within walls of the cerebrovasculature and contributes to intracerebral hemorrhage, ischemic stroke, and cognitive dysfunction in patients with Alzheimers disease (AD) and in non-pathological aging. Previous studies have shown that mTOR drives cerebrovascular dysfunction and cognitive impairment observed in AD, vascular cognitive impairment, and normative aging. However, the mechanisms by which mTOR contributes to CAA are unknown. Here, we show that mTOR drives the accumulation of fibrillar vascular A{beta} lesions in the Tg2576 Model of AD with CAA (using equal numbers of female and male