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Abstract
The renin-angiotensin system (RAS) is an important regulator of blood pressure. Observational
and experimental studies suggest that alterations in blood pressure and components
of the brain RAS contribute to the development and progression of Alzheimer's disease
(AD), resulting in changes that can lead or contribute to cognitive decline. The complexity
of the RAS and diversity of its interactions with neurological processes have recently
become apparent but large gaps in our understanding still remain. Modulation of activity
of components of the brain RAS offers substantial opportunities for the treatment
and prevention of dementia, including AD. This paper reviews molecular, genetic, experimental
and clinical data as well as the therapeutic opportunities that relate to the involvement
of the RAS in AD.