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首页> 外文期刊>CNS & Neurological Disorders - Drug Targets >Role of Glycosphingolipids and Therapeutic Perspectives on Alzheimer's Disease
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Role of Glycosphingolipids and Therapeutic Perspectives on Alzheimer's Disease

机译：糖鞘脂的作用和对阿尔茨海默氏病的治疗观点

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Alzheimer's disease (AD) is a devastating neurodegenerative disorder dividing into two forms, early onset familial and late onset sporadic forms. Early onset genetic cases (familial AD (FAD)) constitute about 10% of all AD cases. Heretofore, highly fibrillinogenic and pathological Aβ peptide formation is regarded as the fundamental molecular basis for this disorder. Recent enormous efforts to find out a pathogenesis, however, have revealed that this disorder has a multiplicity of causes such as glycosphingolipids abnormalities, impairment of neurotrophin signaling, protein trafficking, and protein turnover. Most of these aspects were disclosed by the studies on FAD-related presenilin. In this review, we will focus on the current knowledge of many abnormal aspects of cellular lipids, especially glycosphingolipids other than a pathogenic Aβ production caused by the mutant presenilins as a model system. Moreover, we will discuss how these glycosphingolipids abnormalities cause the pathological conditions found in this disorder.
机译：阿尔茨海默氏病（AD）是一种破坏性神经退行性疾病，分为早期发作的家族性和晚期发作的偶发性两种形式。早期发病的遗传病例（家族性AD（FAD））约占所有AD病例的10％。迄今为止，高原纤维蛋白原性和病理性Aβ肽的形成被认为是该疾病的基本分子基础。然而，最近为发现发病机理所做的巨大努力表明，这种疾病有多种原因，例如糖鞘脂异常，神经营养蛋白信号转导受损，蛋白质运输和蛋白质更新。这些方面中的大多数已通过与FAD相关的早老素的研究公开。在这篇综述中，我们将集中于细胞脂质，尤其是糖鞘脂的许多异常方面的当前知识，而不是由突变的早老蛋白作为模型系统引起的致病性Aβ产生。此外，我们将讨论这些糖鞘脂异常如何导致这种疾病的病理状况。

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