Genomics: New Light on Alzheimer's Disease Research

被引:14
|
作者
Jung, Yeong Ju [1 ]
Kim, Yoon Ha [1 ]
Bhalla, Mridula [2 ]
Lee, Sung Bae [1 ]
Seo, Jinsoo [1 ]
机构
[1] DGIST, Dept Brain & Cognit Sci, Daegu 42988, South Korea
[2] Savitribai Phule Pune Univ, Inst Bioinformat & Biotechnol, Pune 411007, Maharashtra, India
基金
新加坡国家研究基金会;
关键词
alzheimer's disease; genomics; GWAS; genetic risk factors; epigenetic modification; aging; APOLIPOPROTEIN-E; TRANSGENIC MICE; MOUSE MODELS; NEUROFIBRILLARY TANGLES; EPIGENETIC ALTERATIONS; HISTONE ACETYLATION; TREM2; VARIANTS; TYPE-4; ALLELE; NEURONAL LOSS; AGED RATS;
D O I
10.3390/ijms19123771
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alzheimer's disease (AD) is a progressive neurodegenerative disease that represents a major cause of death in many countries. AD is characterized by profound memory loss, disruptions in thinking and reasoning, and changes in personality and behavior followed by malfunctions in various bodily systems. Although AD was first identified over 100 years ago, and tremendous efforts have been made to cure the disease, the precise mechanisms underlying the onset of AD remain unclear. The recent development of next-generation sequencing tools and bioinformatics has enabled us to investigate the role of genetics in the pathogenesis of AD. In this review, we discuss novel discoveries in this area, including the results of genome-wide association studies (GWAS) that have implicated a number of novel genes as risk factors, as well as the identification of epigenetic regulators strongly associated with the onset and progression of AD. We also review how genetic risk factors may interact with age-associated, progressive decreases in cognitive function in patients with AD.
引用
收藏
页数:17
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