Giri Mohan, Zhang Man, Lü Yang
Department of Geriatrics, The First Affiliated Hospital of Chongqing Medical University, Yuzhong District, Chongqing, People's Republic of China.
Clin Interv Aging. 2016 May 17;11:665-81. doi: 10.2147/CIA.S105769. eCollection 2016.
Alzheimer's disease (AD) is a progressive, neurodegenerative disease and the most common form of dementia in elderly people. It is an emerging public health problem that poses a huge societal burden. Linkage analysis was the first milestone in unraveling the mutations in APP, PSEN1, and PSEN2 that cause early-onset AD, followed by the discovery of apolipoprotein E-ε4 allele as the only one genetic risk factor for late-onset AD. Genome-wide association studies have revolutionized genetic research and have identified over 20 genetic loci associated with late-onset AD. Recently, next-generation sequencing technologies have enabled the identification of rare disease variants, including unmasking small mutations with intermediate risk of AD in PLD3, TREM2, UNC5C, AKAP9, and ADAM10. This review provides an overview of the genetic basis of AD and the relationship between these risk genes and the neuropathologic features of AD. An understanding of genetic mechanisms underlying AD pathogenesis and the potentially implicated pathways will lead to the development of novel treatment for this devastating disease.
阿尔茨海默病(AD)是一种进行性神经退行性疾病,也是老年人中最常见的痴呆形式。它是一个新出现的公共卫生问题,带来了巨大的社会负担。连锁分析是揭示导致早发性AD的APP、PSEN1和PSEN2基因突变的第一个里程碑,随后发现载脂蛋白E-ε4等位基因是晚发性AD的唯一遗传风险因素。全基因组关联研究彻底改变了基因研究,并确定了20多个与晚发性AD相关的基因位点。最近,新一代测序技术使得识别罕见病变异成为可能,包括揭示PLD3、TREM2、UNC5C、AKAP9和ADAM10中具有AD中等风险的小突变。本文综述了AD的遗传基础以及这些风险基因与AD神经病理特征之间的关系。了解AD发病机制的遗传机制以及潜在涉及的途径将有助于开发针对这种毁灭性疾病的新疗法。