Molecular genetics of attention deficit hyperactivity disorder.
Molecular genetics of attention deficit hyperactivity disorder.
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DOI：
10.1016/j.psc.2009.12.004
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发表时间：
2010-03
期刊：
影响因子：
--
通讯作者：
Mick E
中科院分区：
文献类型：
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作者：
Faraone SV;Mick E
尽管双胞胎研究表明ADHD是一种高度可遗传的疾病，但分子遗传学研究表明ADHD的遗传结构是复杂的。到目前为止，已经进行的少数全基因组链接和关联扫描显示了不同的发现，因此并不是决定性的。同样，从神经生物学系统的角度来看，许多候选基因(即DBH、MAOA、SLC6A2、TPH-2、SLC6A4、CHRNA4、GRIN2A)在理论上是令人信服的，但现有的数据稀少且不一致。然而，ADHD的候选基因研究已经产生了大量的证据，证实了几个基因在ADHD的病因学中的作用，Meta分析支持编码DRD4、DRD5、SLC6A3、SNAP-25和HTR1B的基因在ADHD的病因学中的作用。
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 (i.e. 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.