PDF(Sci-hub)
Abstract：
Childhood onset aggression can cause major suffering to affected families and is associated with many negative outcomes in the child\'s later life, including poor academic performance, adolescent delinquency, drug abuse, depression and antisocial personality disorder. Currently available prevention and intervention strategies have limited efficacy, but a better understanding of underlying genetic and neurobiological factors can lead to more effective prevention and treatment strategies, through genetic screening programs and novel therapies.
This study examined the RS1 (n = 299 aggression, n = 192 controls) and RS3 (n = 291 aggression, n = 189 controls) microsatellite repeats within the promoter region of the vasopressin receptor 1A gene (AVPR1A) and their association with extreme childhood aggression, as assessed by the Child Behavior Checklist (CBCL), as well as the Teacher Report Form (TRF) and Youth Self Report (YSR). Binary logistic regression was used to model the relationship between microsatellite length and childhood aggression. Age and sex were used as covariates.
Logistic regression revealed a nominally significant association between one specific RS3 repeat and non-aggressive status. No association was found for any of the RS1 repeats. In a separate model, grouping repeats into short and long, carriers of long RS3 repeats were nominally significantly associated with non-aggressive status.
These findings suggest a role for AVPR1A and its RS3 microsatellite in extreme childhood aggression and could lead to a better understanding of the biological pathways of aggressive behavior. However, independent replication and further research into the functionality of studied genetic variants is required.
This study examined the RS1 (n = 299 aggression, n = 192 controls) and RS3 (n = 291 aggression, n = 189 controls) microsatellite repeats within the promoter region of the vasopressin receptor 1A gene (AVPR1A) and their association with extreme childhood aggression, as assessed by the Child Behavior Checklist (CBCL), as well as the Teacher Report Form (TRF) and Youth Self Report (YSR). Binary logistic regression was used to model the relationship between microsatellite length and childhood aggression. Age and sex were used as covariates.
Logistic regression revealed a nominally significant association between one specific RS3 repeat and non-aggressive status. No association was found for any of the RS1 repeats. In a separate model, grouping repeats into short and long, carriers of long RS3 repeats were nominally significantly associated with non-aggressive status.
These findings suggest a role for AVPR1A and its RS3 microsatellite in extreme childhood aggression and could lead to a better understanding of the biological pathways of aggressive behavior. However, independent replication and further research into the functionality of studied genetic variants is required.
摘要：
儿童期发作的攻击会给受影响的家庭带来重大痛苦，并与儿童晚年的许多负面结果有关，包括学习成绩差，青少年犯罪，药物滥用,抑郁症和反社会人格障碍。目前可用的预防和干预策略效果有限，但是更好地了解潜在的遗传和神经生物学因素可以导致更有效的预防和治疗策略，通过基因筛查计划和新疗法。
这项研究检查了RS1(n=299攻击，n=192个对照）和RS3（n=291个攻击性，n=189个对照）在加压素受体1A基因（AVPR1A）的启动子区域内的微卫星重复及其与极端儿童侵略的关联，根据儿童行为清单(CBCL)评估，以及教师报告表（TRF）和青年自我报告（YSR）。使用二元逻辑回归对微卫星长度与儿童攻击性之间的关系进行建模。年龄和性别用作协变量。
Logistic回归显示一个特定的RS3重复和非侵袭性状态之间的名义上显著的关联。没有发现任何RS1重复的关联。在单独的模型中，将重复分为短和长，长RS3重复的携带者名义上与非侵袭性状态显著相关.
这些发现表明AVPR1A及其RS3微卫星在儿童极端攻击中的作用，并可能导致更好地理解攻击行为的生物学途径。然而,需要独立复制和进一步研究所研究的遗传变异的功能。
这项研究检查了RS1(n=299攻击，n=192个对照）和RS3（n=291个攻击性，n=189个对照）在加压素受体1A基因（AVPR1A）的启动子区域内的微卫星重复及其与极端儿童侵略的关联，根据儿童行为清单(CBCL)评估，以及教师报告表（TRF）和青年自我报告（YSR）。使用二元逻辑回归对微卫星长度与儿童攻击性之间的关系进行建模。年龄和性别用作协变量。
Logistic回归显示一个特定的RS3重复和非侵袭性状态之间的名义上显著的关联。没有发现任何RS1重复的关联。在单独的模型中，将重复分为短和长，长RS3重复的携带者名义上与非侵袭性状态显著相关.
这些发现表明AVPR1A及其RS3微卫星在儿童极端攻击中的作用，并可能导致更好地理解攻击行为的生物学途径。然而,需要独立复制和进一步研究所研究的遗传变异的功能。
