4.7 Review

Genomics: New Light on Alzheimer's Disease Research

期刊

出版社

MDPI
DOI: 10.3390/ijms19123771

关键词

alzheimer's disease; genomics; GWAS; genetic risk factors; epigenetic modification; aging

资金

  1. National Research Foundation of Korea (NRF) - Ministry of Science and ICT [18-BD-0402, 18-BT-02, 2018R1A2B6001607]
  2. DGIST R&D Program through the National Research Foundation of Korea (NRF) - Ministry of Science and ICT [18-BD-0402, 18-BT-02, 2018R1A2B6001607]
  3. DGIST MIREBraiN program through the NRF of Korea - Ministry of Education [2018R1D1A1B07046356]
  4. NRF of Korea - Ministry of Education [2018R1D1A1B07046356]
  5. Ministry of Science & ICT (MSIT), Republic of Korea [18-BD-0402] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
  6. National Research Foundation of Korea [2018R1A2B6001607, 2018R1D1A1B07046356] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

向作者/读者索取更多资源

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.

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