Suppr超能文献

迟发性阿尔茨海默病的遗传发现和进展。

Genetic discoveries and advances in late-onset Alzheimer's disease.

机构信息

Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.

Division of Medical Genetics, Tabriz Children's Hospital, Tabriz University of Medical Sciences, Tabriz, Iran.

出版信息

J Cell Physiol. 2019 Aug;234(10):16873-16884. doi: 10.1002/jcp.28372. Epub 2019 Feb 20.

Abstract

Alzheimer's disease (AD) is a heterogeneous disorder with multiple patterns of clinical manifestations. Recently, due to the advance of linkage studies, next-generation sequencing and genome-wide association studies, a large number of putative risk genes for AD have been identified using acquired genome mega data. The genetic association between three causal genes, including amyloid precursor protein, presenilin1, and presenilin2 in early-onset AD (EOAD), was discovered over the past few decades. These discoveries showed that there should be additional genetic risk factors for both EOAD and late-onset AD (LOAD) to help fully explain the leading molecular mechanisms in a single pathophysiological entity. This study reviews the clinical features and genetic etiology of LOAD and discusses a variety of AD-mediated genes that are involved in cholesterol and lipid metabolism, endocytosis, and immune response according to their mutations for more efficient selection of functional candidate genes for LOAD. New mechanisms and pathways have been identified as a result.

摘要

阿尔茨海默病(AD)是一种具有多种临床表现模式的异质性疾病。最近,由于连锁研究、下一代测序和全基因组关联研究的进展,利用获得的基因组大数据,已经确定了大量 AD 的潜在风险基因。在过去的几十年中,发现了三个因果基因(包括淀粉样前体蛋白、早发性 AD(EOAD)中的早老素 1 和早老素 2)之间的遗传关联。这些发现表明,EOAD 和迟发性 AD(LOAD)都应该有其他遗传风险因素,以帮助充分解释单一病理生理实体中的主要分子机制。本研究回顾了 LOAD 的临床特征和遗传病因,并根据其突变讨论了多种与 AD 相关的参与胆固醇和脂质代谢、内吞作用和免疫反应的基因,以便更有效地选择 LOAD 的功能候选基因。结果发现了新的机制和途径。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验