Genetic and Environmental Influences on the Developmental Course of Attention-Deficit/Hyperactivity Disorder Symptoms From Childhood to Adolescence.
Genetic and Environmental Influences on the Developmental Course of Attention-Deficit/Hyperactivity Disorder Symptoms From Childhood to Adolescence.
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DOI：
10.1001/jamapsychiatry.2015.0469
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发表时间：
2015-07
期刊：
影响因子：
25.8
通讯作者：
Rijsdijk F
中科院分区：
文献类型：
--
作者：
Pingault JB;Viding E;Galéra C;Greven CU;Zheng Y;Plomin R;Rijsdijk F
注意力缺陷多动障碍（ADHD）被认为是一种具有强烈遗传性的神经发育障碍。然而，据我们所知，迄今为止，还没有研究探讨遗传和环境的影响，解释从儿童到青春期ADHD症状的发展过程中的个体间差异（即，系统的减少或增加随着年龄的增长）。ADHD症状在一些儿童中持续存在，但在其他儿童中下降的原因是一个重要的问题，对预后和干预措施有影响。评估基因和环境对8 - 16岁ADHD多动/冲动和注意力不集中症状域发育过程中个体间差异的比例影响。双胞胎早期发育研究的8395对双胞胎前瞻性样本，从1994年1月1日至1996年12月31日期间英格兰和威尔士出生人口记录中招募。2002年11月至2004年11月收集了8岁时的数据; 2011年2月至2013年1月收集了16岁时的数据。两个DSM-IV ADHD症状分量表都被参与者的母亲评定了4次。潜在生长曲线模型的估计值表明，多动症/冲动症状的发展过程遵循急剧的线性下降（平均评分为6.0，8岁至2.9，16岁）。多动/冲动性线性变化的个体间差异受强加性遗传影响（81%; 95%CI，73%-88%）。超过一半的遗传变异是特定的发展过程，而不是共享的基线水平的多动/冲动。注意力不集中症状的线性下降不太明显（8岁时平均评分为5.8，16岁时为4.9）。非加性遗传影响占注意力不集中症状发展过程中的大量变异（54%; 95%CI，8%-76%），其中一半以上是特定于发展过程。对ADHD症状发展过程的大的遗传影响大多是特异性的，并且独立于那些解释症状基线水平变化的遗传影响。不同的基因组可能与ADHD症状的发展过程和基线水平有关，并解释了为什么有些儿童从ADHD中缓解，而另一些儿童则持续存在。最近的纵向成像数据表明，症状的维持或增加是由皮质发育的非典型轨迹所支撑的。这可能反映了一种特定的遗传易感性，与导致基线ADHD症状的遗传易感性不同，需要更密切的随访。
Attention-deficit/hyperactivity disorder (ADHD) is conceptualized as a neurodevelopmental disorder that is strongly heritable. However, to our knowledge, no study to date has examined the genetic and environmental influences explaining interindividual differences in the developmental course of ADHD symptoms from childhood to adolescence (ie, systematic decreases or increases with age). The reason ADHD symptoms persist in some children but decline in others is an important concern, with implications for prognosis and interventions. To assess the proportional impact of genes and the environment on interindividual differences in the developmental course of ADHD symptom domains of hyperactivity/impulsivity and inattention between ages 8 and 16 years. A prospective sample of 8395 twin pairs from the Twins Early Development Study, recruited from population records of births in England andWales between January 1, 1994, and December 31, 1996. Data collection at age 8 years took place between November 2002 and November 2004; data collection at age 16 years took place between February 2011 and January 2013. Both DSM-IV ADHD symptom subscales were rated 4 times by participants’ mothers. Estimates from latent growth curve models indicated that the developmental course of hyperactivity/impulsivity symptoms followed a sharp linear decrease (mean score of 6.0 at age 8 years to 2.9 at age 16 years). Interindividual differences in the linear change in hyperactivity/impulsivity were under strong additive genetic influences (81%; 95% CI, 73%-88%). More than half of the genetic variation was specific to the developmental course and not shared with the baseline level of hyperactivity/impulsivity. The linear decrease in inattention symptoms was less pronounced (mean score of 5.8 at age 8 years to 4.9 at age 16 years). Nonadditive genetic influences accounted for a substantial amount of variation in the developmental course of inattention symptoms (54%; 95% CI, 8%-76%), with more than half being specific to the developmental course. The large genetic influences on the developmental course of ADHD symptoms are mostly specific and independent of those that account for variation in the baseline level of symptoms. Different sets of genes may be associated with the developmental course vs the baseline level of ADHD symptoms and explain why some children remit from ADHD, whereas others persist. Recent longitudinal imaging data indicate that the maintenance or increase in symptoms is underpinned by atypical trajectories of cortical development. This may reflect a specific genetic liability, distinct from that which contributes to baseline ADHD symptoms, and warrants closer follow-up.