Corrigendum to "Childhood maltreatment, behavioral adjustment, and molecular markers of cellular aging in preschool-aged children: A cohort study" [Psychoneuroendocrinology 107 (2019) 261-269].
Corrigendum to "Childhood maltreatment, behavioral adjustment, and molecular markers of cellular aging in preschool-aged children: A cohort study" [Psychoneuroendocrinology 107 (2019) 261-269].
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“学龄前儿童的童年虐待、行为调整和细胞衰老的分子标记:队列研究”的勘误表 [Psychoneuroendocrinology 107 (2019) 261-269]。
DOI:
10.1016/j.psyneuen.2019.104466
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发表时间:
2019
影响因子:
3.7
通讯作者:
Tyrka,AudreyR
中科院分区:
文献类型:
--
作者:
Ridout,KathrynK;Parade,StephanieH;Kao,Hung-Teh;Magnan,Stevie;Seifer,Ronald;Porton,Barbara;Price,LawrenceH;Tyrka,AudreyR
ObjectiveChildhood maltreatment is a major risk factor for the development of behavioral problems and poor physical and mental health. Accelerated cellular aging, through reduced telomere length and mitochondrial dysfunction, may be a mechanism underlying these associations.MethodsFamilies with (n = 133) and without (n = 123) child welfare documentation of moderate-severe maltreatment in the past six months participated in this study. Children ranged in age from 3 to 5 years, were racially and ethnically diverse, and 91% qualified for public assistance. Structured record review and interviews were used to assess a history of maltreatment and other adversities. Telomere length and mitochondrial DNA copy number (mtDNAcn) were measured from saliva DNA using real-time PCR. Measures were repeated at a six-month follow-up assessment. Repeated measures general linear models were used to examine the effects of maltreatment and other adversities on telomere length and mtDNAcn over time.ResultsMaltreatment and other adverse experiences were significant positive predictors of both telomere length and mtDNAcn over time. Internalizing and externalizing behavior problems were also both significantly associated with telomere length, but only internalizing symptoms were associated with mtDNAcn.ConclusionsThis is the first study to show that mtDNAcn is altered in children with stress and trauma, and the findings are consistent with recent studies of adults. Surprisingly, children who experienced moderate-severe levels of maltreatment in the prior six months had longer telomeres, possibly reflecting compensatory changes in response to recent trauma. Telomere length and mtDNAcn were also associated with behavioral problems, suggesting that these measures of cellular aging may be causally implicated in the pathophysiology of stress-related conditions.