期刊
NEUROTHERAPEUTICS
卷 10, 期 4, 页码 664-676出版社
SPRINGER
DOI: 10.1007/s13311-013-0206-5
关键词
DNA methylation; Histone code; Chromatin remodeling; Noncoding RNA; microRNA; Huntington's disease; Therapeutics
资金
- NIH NS [067283-02]
- WCU Neurocytomics Program Grant [800-20080848]
- SRC Grant from National Research Foundation [2010-0029-403]
- Flagship Grant from KIST
- National Research Council of Science & Technology (NST), Republic of Korea [2E24183] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Huntington's disease (HD) is an incurable and fatal hereditary neurodegenerative disorder of mid-life onset characterized by chorea, emotional distress, and progressive cognitive decline. HD is caused by an expansion of CAG repeats coding for glutamine (Q) in exon 1 of the huntingtin gene. Recent studies suggest that epigenetic modifications may play a key role in HD pathogenesis. Alterations of the epigenetic histone code lead to chromatin remodeling and deregulation of neuronal gene transcription that are prominently linked to HD pathogenesis. Furthermore, specific noncoding RNAs and microRNAs are associated with neuronal damage in HD. In this review, we discuss how DNA methylation, post-translational modifications of histone, and noncoding RNA function are affected and involved in HD pathogenesis. In addition, we summarize the therapeutic effects of histone deacetylase inhibitors and DNA binding drugs on epigenetic modifications and neuropathological sequelae in HD. Our understanding of the role of these epigenetic mechanisms may lead to the identification of novel biological markers and new therapeutic targets to treat HD.
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