The role of Beta-adrenergic receptor blockers in Alzheimer's disease: potential genetic and cellular signaling mechanisms
- PMID: 23689075
- PMCID: PMC10852699
- DOI: 10.1177/1533317513488924
The role of Beta-adrenergic receptor blockers in Alzheimer's disease: potential genetic and cellular signaling mechanisms
Abstract
According to genetic studies, Alzheimer's disease (AD) is linked to beta-adrenergic receptor blockade through numerous factors, including human leukocyte antigen genes, the renin-angiotensin system, poly(adenosine diphosphate-ribose) polymerase 1, nerve growth factor, vascular endothelial growth factor, and the reduced form of nicotinamide adenine dinucleotide phosphate. Beta-adrenergic receptor blockade is also implicated in AD due to its effects on matrix metalloproteinases, mitogen-activated protein kinase pathways, prostaglandins, cyclooxygenase-2, and nitric oxide synthase. Beta-adrenergic receptor blockade may also have a significant role in AD, although the role is controversial. Behavioral symptoms, sex, or genetic factors, including Beta 2-adrenergic receptor variants, apolipoprotein E, and cytochrome P450 CYP2D6, may contribute to beta-adrenergic receptor blockade modulation in AD. Thus, the characterization of beta-adrenergic receptor blockade in patients with AD is needed.
Keywords: Alzheimer’s disease; beta-adrenergic receptor antagonism; beta-adrenergic receptor blocker; dementia.
Conflict of interest statement
The authors declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.
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