胆固醇细胞内转运改变与散发性阿尔茨海默病病理特征的发展
Altered Cholesterol Intracellular Trafficking and the Development of Pathological Hallmarks of Sporadic AD.
作者信息
Chen Xuesong, Hui Liang, Soliman Mahmoud L, Geiger Jonathan D
出版信息
J Parkinsons Dis Alzheimers Dis. 2014;1(1). doi: 10.13188/2376-922x.1000002.
Compared to the rare familial early onset Alzheimer's disease (AD) that results from gene mutations in AbPP and presenilin-1, the pathogenesis of sporadic AD is much more complex and is believed to result from complex interactions between nutritional, environmental, epigenetic and genetic factors. Among those factors, the presence APOE4 is still the single strongest genetic risk factor for sporadic AD. However, the exact underlying mechanism whereby apoE4 contributes to the pathogenesis of sporadic AD remains unclear. Here, we discuss how altered cholesterol intracellular trafficking as a result of apoE4 might contribute to the development of pathological hallmarks of AD including brain deposition of amyloid beta (Ab), neurofibrillary tangles, and synaptic dysfunction.
与由淀粉样前体蛋白（APP）和早老素-1基因突变导致的罕见家族性早发性阿尔茨海默病（AD）相比，散发性AD的发病机制要复杂得多，被认为是营养、环境、表观遗传和遗传因素之间复杂相互作用的结果。在这些因素中，APOE4的存在仍然是散发性AD最强的单一遗传风险因素。然而，载脂蛋白E4（apoE4）导致散发性AD发病的确切潜在机制仍不清楚。在此，我们讨论apoE4导致的细胞内胆固醇转运改变如何可能促成AD病理特征的发展，包括β淀粉样蛋白（Aβ）脑沉积、神经原纤维缠结和突触功能障碍。
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