注意缺陷多动障碍的分子遗传学。
Molecular genetics of attention deficit hyperactivity disorder.
机构信息
Department of Psychiatry and Behavioral Sciences, SUNY Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210-2375, USA.
出版信息
Psychiatr Clin North Am. 2010 Mar;33(1):159-80. doi: 10.1016/j.psc.2009.12.004.
Abstract
Although twin studies demonstrate that ADHD is a highly heritable condition, molecular genetic studies suggest that the genetic architecture of ADHD is complex. The handful of genome-wide linkage and association scans that have been conducted thus far show divergent findings and are, therefore, not conclusive. Similarly, many of the candidate genes reviewed here (ie, DBH, MAOA, SLC6A2, TPH-2, SLC6A4, CHRNA4, GRIN2A) are theoretically compelling from neurobiological systems perspective but available data are sparse and inconsistent. However, candidate gene studies of ADHD have produced substantial evidence implicating several genes in the etiology of the disorder, with meta-analyses supportive of a role of the genes coding for DRD4, DRD5, SLC6A3, SNAP-25, and HTR1B in the etiology of ADHD.
摘要
虽然双胞胎研究表明 ADHD 是一种高度遗传性疾病，但分子遗传学研究表明 ADHD 的遗传结构很复杂。迄今为止进行的少数几项全基因组连锁和关联扫描显示出不同的发现，因此没有定论。同样，这里回顾的许多候选基因（即 DBH、MAOA、SLC6A2、TPH-2、SLC6A4、CHRNA4、GRIN2A）从神经生物学系统的角度来看具有理论上的说服力，但可用数据稀疏且不一致。然而，ADHD 的候选基因研究已经提供了大量证据，表明该疾病的病因涉及多个基因，荟萃分析支持 DRD4、DRD5、SLC6A3、SNAP-25 和 HTR1B 基因在 ADHD 病因学中的作用。
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