摘要
阿尔茨海默病(AD)是最常见的痴呆神经退行性疾病,因为我们都知道ApoE4是迟发性阿尔茨海默病(LOAD)的最大遗传风险因素。冠心病(CHD)导致工业化国家死亡人数的四分之一,据报道,ApoE4也增加了患冠心病的风险。此外,有证据表明冠心病也会增加阿尔茨海默病的发病率。 ApoE4是否是连接AD与CHD的桥梁?什么是特殊的机制和治疗方法?研究人员发现,胆固醇代谢紊乱是AD和CHD的常见原因和危险因素。流行病学研究表明,ApoE4等位基因的携带者具有较高的胆固醇血浆浓度。更多证据表明,高胆固醇血症加速冠状动脉粥样硬化的进展,损害中枢神经系统的血脑屏障,促进Aβ蛋白的产生和脑中的Tau沉积。因此,ApoE4可能是AD和CHD之间的桥梁,并且可能是潜在有希望的治疗靶标。
关键词: ApoE4,冠心病(CHD),阿尔茨海默病(AD),中枢神经系统,高胆固醇血症,心血管疾病
图形摘要
Current Drug Targets
Title:ApoE4 May be a Promising Target for Treatment of Coronary Heart Disease and Alzheimer's Disease
Volume: 19 Issue: 9
关键词: ApoE4,冠心病(CHD),阿尔茨海默病(AD),中枢神经系统,高胆固醇血症,心血管疾病
摘要: Alzheimer disease (AD) is most common neurodegenerative disorder of dementia, as we all know that ApoE4 is the greatest genetic risk factor of late-onset Alzheimer's disease (LOAD). Coronary heart disease (CHD) leads to one-fourth of all deaths in industrialized countries, it is reported that ApoE4 increases the risk of coronary heart disease as well. Furthermore, evidence show that coronary heart disease also increases the incidence of Alzheimer's disease. Whether ApoE4 is a bridge connecting AD with CHD or not? And what are the special mechanism and therapeutic methods? Researchers found that cholesterol metabolic disorder is the common cause and risk factor of AD and CHD. Epidemiological studies demonstrate that carriers of the ApoE4 allele have higher cholesterol plasma concentration. More evidence indicate that hypercholesterolemia accelerates the progression of coronary atherosclerosis, damages the central nervous system blood-brain barrier, promotes Aβ protein production and Tau deposition in brain. Therefore, ApoE4 is likely to be the bridge between AD and CHD, and may be a potentially promising therapeutic target.
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Cite this article as:
ApoE4 May be a Promising Target for Treatment of Coronary Heart Disease and Alzheimer's Disease, Current Drug Targets 2018; 19 (9) . https://dx.doi.org/10.2174/1389450119666180406112050
DOI https://dx.doi.org/10.2174/1389450119666180406112050 |
Print ISSN 1389-4501 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-5592 |
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