Partial loss of endothelial nitric oxide leads to increased cerebrovascular beta amyloid.

ABSTRACT: Cerebral amyloid angiopathy (CAA) is present in over half of the elderly population and in 80-90% of Alzheimer's disease (AD) patients. CAA is defined by the deposition of beta amyloid (Aβ) in small cerebral arteries and capillaries. Cardiovascular risk factors are associated with an increased incidence of CAA. We utilized 18-month-old endothelial nitric oxide synthase (eNOS) heterozygous knockout (^+/-) mice, a clinically relevant model of endothelial dysfunction, to examine the role of endothelial nitric oxide (NO) in vascular Aβ accumulation. eNOS^+/- mice had significantly higher vascular levels of Aβ40 (P < 0.05). Aβ42 was not detected. There was no difference in Aβ in brain tissue. Amyloid precursor protein and β-site APP cleavage enzyme 1 protein levels we

SUBMITTER: Austin SA 

PROVIDER: S-EPMC7370614 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature