Epigenetic Mechanisms in Autism Spectrum Disorder

被引:34
|
作者
Zhubi, Adrian [1 ]
Cook, Edwin H. [2 ]
Guidotti, Alessandro [1 ]
Grayson, Dennis R. [1 ]
机构
[1] Univ Illinois, Dept Psychiat, Inst Psychiat, Chicago, IL 60612 USA
[2] Univ Illinois, Dept Psychiat, Inst Juvenile Res, Chicago, IL 60612 USA
来源
EPIGENETICS | 2014年 / 115卷
关键词
CEREBELLAR PURKINJE-CELLS; ANGELMAN SYNDROME GENE; IN-UTERO EXPOSURE; R-LOOP FORMATION; DNA METHYLATION; VALPROIC ACID; CPG ISLANDS; MOUSE MODEL; NEUROTROPHIC FACTOR; PRENATAL EXPOSURE;
D O I
10.1016/B978-0-12-801311-3.00006-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by impaired social interactions, language deficits, as well as restrictive or repetitive behaviors. ASD is clinically heterogeneous with a complex etiopathogenesis which may be conceptualized as a dynamic interplay between heterogeneous environmental cues and predisposing genetic factors involving complex epigenetic mechanisms. Inherited and de novo copy number variants provide novel information regarding genes contributing to ASD. Epigenetic marks are stable, yet potentially reversible, chromatin modifications that alter gene expression profiles by locally changing the degree of nucleosomal compaction, thereby opening or closing promoter access to the transcriptional machinery. Here, we review progress on studies designed to provide a better understanding of how epigenetic mechanisms impact transcriptional programs operative in the brain that contribute to ASD.
引用
收藏
页码:203 / 244
页数:42
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