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Genetics and epigenetics of bipolar disorder (2012)_香港中文大学

香港中文大学 辅仁网/2017-06-25

Genetics and epigenetics of bipolar disorder
Publication in refereed journal


香港中文大学研究人员 ( 现职)
韦妙宜教授 (那打素护理学院)


全文


引用次数
Scopushttp://aims.cuhk.edu.hk/converis/portal/Publication/0Scopus source URL

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摘要Bipolar disorder (BD), also known as manic depression, is a severe mood disorder that causes shifts in mood, energy and ability to function. While there is no cure currently, many people with bipolar disorder could be treated and with the right medication, could go into remission and be symptom free for years or decades. It is estimated that BD affects 2.4% of the population worldwide. Patients of BD suffer from recurrent episodes of mania and depression with each episode typically lasting for 1 to 2 weeks. As a result, patients' lives are severely disrupted. Studies have shown that it is a complex mental disease which is highly heritable, polygenic yet multifactorial. So far vast numbers of candidate genes have been implicated for BD and several models have been proposed to explain the pathology of BD: ion channel pathology (ANK3, CACNA1C and GABRB2), disruption of signaling pathways (BDNF, DGKH, NTRK2 and NRG1), abnormal cell-cell adhesion (FAT1, CTNNA2, CDH7 and NCAN), and disruption in circadian rhythm (CLOCK, ARNNTL and TIMELESS). Concerning the epigenetic studies of BD, differential DNA methylation has been observed in both coding genes (HTR1A, MB-COMT CTNNA2 and MHR1) and non-protein coding gene (HCG9). In addition to specific gene candidates, some studies attempt to find the link between BD and epigenetic modification.

着者Yeung M., Waye M.
期刊名称Journal of Biochemistry and Molecular Biology in the Post Genomic Era
丛书册次2
出版年份2http://aims.cuhk.edu.hk/converis/portal/Publication/012
卷号2
出版社Nova Science Publishers, Inc.
页次71 - 1http://aims.cuhk.edu.hk/converis/portal/Publication/0http://aims.cuhk.edu.hk/converis/portal/Publication/0
国际标準书号9781634823128
国际标準期刊号2156-5732
语言美式英语

关键词Association study, Cell adhesion, DNA methylation, GWAS, Ion channel, Signaling pathway, SNPs

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