Vietnamese American Medical Research Foundation, Westminster, California, CA 92683, USA.
Am J Alzheimers Dis Other Demen. 2013 Aug;28(5):427-39. doi: 10.1177/1533317513488924. Epub 2013 May 20.
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.
根据遗传研究,阿尔茨海默病(AD)通过多种因素与β-肾上腺素能受体阻断有关,包括人类白细胞抗原基因、肾素-血管紧张素系统、多聚(腺嘌呤二核苷酸核糖)聚合酶 1、神经生长因子、血管内皮生长因子和烟酰胺腺嘌呤二核苷酸磷酸的还原形式。β-肾上腺素能受体阻断也与 AD 有关,因为它对基质金属蛋白酶、有丝分裂原激活蛋白激酶途径、前列腺素、环氧化酶-2 和一氧化氮合酶有影响。β-肾上腺素能受体阻断在 AD 中也可能具有重要作用,尽管作用存在争议。行为症状、性别或遗传因素,包括β2-肾上腺素能受体变体、载脂蛋白 E 和细胞色素 P450 CYP2D6,可能有助于 AD 中β-肾上腺素能受体阻断的调节。因此,需要对 AD 患者的β-肾上腺素能受体阻断进行特征描述。