Genetics of attention deficit hyperactivity disorder

被引:670
作者
Faraone, Stephen V. [1 ,2 ]
Larsson, Henrik [3 ,4 ]
机构
[1] SUNY Upstate Med Univ, Dept Psychiat, Syracuse, NY 13210 USA
[2] SUNY Upstate Med Univ, Dept Neurosci & Physiol, Syracuse, NY 13210 USA
[3] Orebro Univ, Sch Med Sci, Orebro, Sweden
[4] Karolinska Inst, Dept Med Epidemiol & Biostat, Stockholm, Sweden
基金
瑞典研究理事会;
关键词
GENOME-WIDE ASSOCIATION; COPY NUMBER VARIANTS; OPPOSITIONAL DEFIANT DISORDER; AUTISM SPECTRUM DISORDERS; POPULATION-BASED SAMPLE; DEFICIT/HYPERACTIVITY DISORDER; ADHD SYMPTOMS; ENVIRONMENTAL CONTRIBUTIONS; CONDUCT DISORDER; MOLECULAR-GENETICS;
D O I
10.1038/s41380-018-0070-0
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Decades of research show that genes play an vital role in the etiology of attention deficit hyperactivity disorder (ADHD) and its comorbidity with other disorders. Family, twin, and adoption studies show that ADHD runs in families. ADHD's high heritability of 74% motivated the search for ADHD susceptibility genes. Genetic linkage studies show that the effects of DNA risk variants on ADHD must, individually, be very small. Genome-wide association studies (GWAS) have implicated several genetic loci at the genome-wide level of statistical significance. These studies also show that about a third of ADHD's heritability is due to a polygenic component comprising many common variants each having small effects. From studies of copy number variants we have also learned that the rare insertions or deletions account for part of ADHD's heritability. These findings have implicated new biological pathways that may eventually have implications for treatment development.
引用
收藏
页码:562 / 575
页数:14
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