Roles of β-adrenergic receptors in Alzheimer's disease: implications for novel therapeutics

Abstract

Alzheimer's disease (AD), the most common cause of age-related dementia, is a progressive neurodegenerative disorder with an enormous unmet medical need. In recent years, several unexpected longitudinal and cross-sectional epidemiological studies reveal that beta-blockers treatment reduces the prevalence of AD in patients suffering from hypertension. Now, a newly population-based study of individuals with incident AD demonstrates that beta-blockers are also associated with delay of functional decline. Furthermore, accumulated convincing evidences from cell culture experiments and animal studies have also suggested that β-adrenergic receptors (β-ARs) may involve in the AD pathogenesis through effects on amyloid-β (Aβ) production or inflammation. This review explores clinical and experimental studies that might help to explain the roles of β-ARs in the AD pathogenesis and the potential underlying mechanisms and whether treatment with β-ARs antagonists provides a new therapeutic option for AD.