Reynolds Oklahoma Center on Aging, Donald W. Reynolds Department of Geriatric Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma;
Am J Physiol Heart Circ Physiol. 2013 Oct 15;305(8):H1120-30. doi: 10.1152/ajpheart.00288.2013. Epub 2013 Aug 16.
Strong epidemiological and experimental evidence indicate that hypertension in the elderly predisposes to the development of Alzheimer's disease (AD), but the underlying mechanisms remain elusive. The present study was designed to characterize the additive/synergistic effects of hypertension and aging on the expression of genes involved in β-amyloid generation and AD in the hippocampus, an area of brain contributing to higher cognitive function, which is significantly affected by AD both in humans and in mouse models of the disease. To achieve that goal, we induced hypertension in young (3 mo) and aged (24 mo) C57BL/6 mice by chronic (4 wk) infusion of angiotensin II and assessed changes in hippocampal mRNA expression of genes involved in amyloid precursor protein (APP)-dependent signaling, APP cleavage, Aβ processing and Aβ-degradation, synaptic function, dysregulation of microtubule-associated τ protein, and apolipoprotein-E signaling. Aged hypertensive mice exhibited spatial memory impairments in the Y-maze and impaired performance in the novel object recognition assay. Surprisingly, hypertension in aging did not increase the expression of APP, β- and γ-secretases, or genes involved in tauopathy. These genes are all involved in the early onset form of AD. Yet, hypertension in aging was associated with changes in hippocampal expression of APP binding proteins, e.g., [Mint3/amyloid β A4 precursor protein-binding family A member 3 (APBA3), Fe65/amyloid β A4 precursor protein-binding family B member 1 (APBB1)], amyloid β (A4) precursor-like protein 1 (APLP1), muscarinic M1 receptor, and serum amyloid P component, all of which may have a role in the pathogenesis of late-onset AD. The hippocampal gene expression signature observed in aged hypertensive mice in the present study provides important clues for subsequent studies to elucidate the mechanisms by which hypertension may contribute to the pathogenesis and clinical manifestation of AD.
强有力的流行病学和实验证据表明,老年人的高血压会导致阿尔茨海默病(AD)的发生,但潜在机制仍不清楚。本研究旨在描述高血压和衰老对海马中参与β-淀粉样蛋白生成和 AD 的基因表达的叠加/协同作用,海马是大脑中有助于更高认知功能的区域,在人类和 AD 疾病的小鼠模型中,该区域都受到显著影响。为了实现这一目标,我们通过慢性(4 周)输注血管紧张素 II 在年轻(3 个月)和老年(24 个月)C57BL/6 小鼠中诱导高血压,并评估了与 APP 依赖性信号、APP 切割、Aβ 加工和 Aβ 降解、突触功能、微管相关 tau 蛋白失调以及载脂蛋白-E 信号相关的基因在海马中的 mRNA 表达变化。患有高血压的老年小鼠在 Y 迷宫中表现出空间记忆障碍,并在新物体识别试验中表现出运动障碍。令人惊讶的是,衰老中的高血压并没有增加 APP、β-和 γ-分泌酶或参与 tau 病的基因的表达。这些基因都参与了 AD 的早期发病形式。然而,衰老中的高血压与海马中 APP 结合蛋白的表达变化有关,例如 [Mint3/淀粉样β A4 前体蛋白结合家族 A 成员 3(APBA3)、Fe65/淀粉样β A4 前体蛋白结合家族 B 成员 1(APBB1)]、淀粉样β(A4)前体样蛋白 1(APLP1)、毒蕈碱 M1 受体和血清淀粉样蛋白 P 成分,所有这些都可能在迟发性 AD 的发病机制中发挥作用。本研究中观察到的老年高血压小鼠海马基因表达谱为后续研究提供了重要线索,以阐明高血压如何导致 AD 的发病机制和临床表现。