Molecular genetics of adult ADHD: converging evidence from genome-wide association and extended pedigree linkage studies
Molecular genetics of adult ADHD: converging evidence from genome-wide association and extended pedigree linkage studies
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DOI：
10.1007/s00702-008-0119-3
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发表时间：
2008-11-01
影响因子：
3.3
通讯作者：
Jacob, Christian
中科院分区：
文献类型：
--
作者：
Lesch, Klaus-Peter;Timmesfeld, Nina;Jacob, Christian
一项在成人注意力缺陷/多动障碍(ADHD)中使用类似于500K SNP标记的全基因组关联(GWA)研究发现了新的危险基因，并揭示了与最近GWA扫描结果在物质使用障碍中的显著重叠。与我们之前报道的扩展家系高分辨率连锁扫描的结果相比，证实了几个染色体座位，包括16q23.1-24.3，在最近对七个连锁研究进行的荟萃分析中也达到了全基因组意义(周等人。见Am J Med Genet Part B，2008)。这些发现为编码细胞黏附分子(例如CDH13、ASTN2)和突触可塑性调节因子(例如CTNNA2、KALRN)的基因的共同作用提供了额外的支持，尽管成人ADHD和成瘾易感性存在复杂的多因素病因。
A genome-wide association (GWA) study with pooled DNA in adult attention-deficit/hyperactivity disorder (ADHD) employing similar to 500K SNP markers identifies novel risk genes and reveals remarkable overlap with findings from recent GWA scans in substance use disorders. Comparison with results from our previously reported high-resolution linkage scan in extended pedigrees confirms several chromosomal loci, including 16q23.1-24.3 which also reached genome-wide significance in a recent meta-analysis of seven linkage studies (Zhou et al. in Am J Med Genet Part B, 2008). The findings provide additional support for a common effect of genes coding for cell adhesion molecules (e.g., CDH13, ASTN2) and regulators of synaptic plasticity (e.g., CTNNA2, KALRN) despite the complex multifactorial etiologies of adult ADHD and addiction vulnerability.