APOE4在阿尔茨海默病中的作用:未来治疗干预策略

Q4 Neuroscience Neuronal signaling Pub Date : 2019-06-01 Epub Date: 2019-04-18 DOI:10.1042/NS20180203
Holly C Hunsberger, Priyanka D Pinky, Warren Smith, Vishnu Suppiramaniam, Miranda N Reed
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引用次数: 24

摘要

阿尔茨海默病(AD)是导致痴呆症的主要原因,影响全世界近5000万人。载脂蛋白E (APOE)的ε4等位基因是已知的迟发性AD病例的最强遗传危险因素,纯合子APOE4携带者患该病的可能性约为15倍。25%的人群携带APOE4,了解该等位基因在AD发病机制和病理生理中的作用至关重要。虽然ε4等位基因增加AD风险的确切机制尚不清楚,但APOE介导的过程,包括胆固醇转运、突触形成、神经突生长调节、突触可塑性、微管不稳定和β-淀粉样蛋白清除,提示了潜在的治疗靶点。本文将对APOE对神经元和神经元信号传导的影响、APOE与AD病理的相互作用以及与记忆衰退的关系进行综述。然后,我们将描述目前针对APOE4的治疗方法,与当前治疗方法相关的并发症,以及对未来研究和治疗领域的建议。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

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The role of APOE4 in Alzheimer's disease: strategies for future therapeutic interventions.

Alzheimer's disease (AD) is the leading cause of dementia affecting almost 50 million people worldwide. The ε4 allele of Apolipoprotein E (APOE) is the strongest known genetic risk factor for late-onset AD cases, with homozygous APOE4 carriers being approximately 15-times more likely to develop the disease. With 25% of the population being APOE4 carriers, understanding the role of this allele in AD pathogenesis and pathophysiology is crucial. Though the exact mechanism by which ε4 allele increases the risk for AD is unknown, the processes mediated by APOE, including cholesterol transport, synapse formation, modulation of neurite outgrowth, synaptic plasticity, destabilization of microtubules, and β-amyloid clearance, suggest potential therapeutic targets. This review will summarize the impact of APOE on neurons and neuronal signaling, the interactions between APOE and AD pathology, and the association with memory decline. We will then describe current treatments targeting APOE4, complications associated with the current therapies, and suggestions for future areas of research and treatment.

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来源期刊
CiteScore
4.60
自引率
0.00%
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审稿时长
14 weeks
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