Swartz Johnna R, Williamson Douglas E, Hariri Ahmad R
From the Center for Developmental Science, University of North Carolina at Chapel Hill; the Department of Psychology and Neuroscience and the Institute for Genome Sciences and Policy, Duke University, Durham, N.C.; and the Translational Epidemiology Program, Department of Psychiatry, University of Texas Health Sciences Center at San Antonio.
Am J Psychiatry. 2015 Mar 1;172(3):276-83. doi: 10.1176/appi.ajp.2014.14020195. Epub 2014 Dec 19.
Although heightened amygdala reactivity is observed in patients with major depression, two critical gaps in our knowledge remain. First, it is unclear whether heightened amygdala reactivity is a premorbid vulnerability or a consequence of the disorder. Second, it is unknown how and when this neural phenotype develops. The authors sought to address these gaps by evaluating developmental change in threat-related amygdala reactivity in adolescents at high or low risk for depression based on family history, before onset of disorder.
At baseline and again 2 years later, adolescents (initially 11-15 years of age) participated in a functional MRI paradigm that elicited threat-related amygdala reactivity. After quality control, data were available for 232 adolescents at wave 1 and 197 adolescents at wave 2; longitudinal data meeting quality control at both waves were available for 157 of these participants. Change in amygdala reactivity was assessed as a function of family history of depression and severity of stressful life events.
Threat-related amygdala reactivity increased with age in participants with a positive family history regardless of the severity of life stress reported, and it increased in adolescents with a negative family history who reported relatively severe life stress. These changes in amygdala reactivity with age occurred in the absence of clinical disorder or increases in depressive symptoms.
These results suggest that heightened amygdala reactivity emerges during adolescence, prior to the development of depression, as a function of familial risk or, in the absence of familial risk, stressful life events.
尽管在重度抑郁症患者中观察到杏仁核反应性增强,但我们的认知仍存在两个关键空白。首先,尚不清楚杏仁核反应性增强是病前易感性还是该疾病的后果。其次,这种神经表型如何以及何时发展尚不清楚。作者试图通过评估基于家族史在抑郁症发作前处于高风险或低风险的青少年中与威胁相关的杏仁核反应性的发育变化来填补这些空白。
在基线时以及两年后,青少年(最初年龄为11 - 15岁)参与了一种功能性磁共振成像范式,该范式引发与威胁相关的杏仁核反应性。经过质量控制后,第1波有232名青少年的数据可用,第2波有197名青少年的数据可用;其中157名参与者在两波中均符合质量控制的纵向数据可用。杏仁核反应性的变化被评估为抑郁症家族史和应激性生活事件严重程度的函数。
无论报告的生活压力严重程度如何,有阳性家族史的参与者中与威胁相关的杏仁核反应性随年龄增加,而在报告相对严重生活压力的有阴性家族史的青少年中也增加。杏仁核反应性随年龄的这些变化发生在没有临床疾病或抑郁症状增加的情况下。
这些结果表明,在抑郁症发展之前的青春期,杏仁核反应性增强作为家族风险的函数出现,或者在没有家族风险的情况下,作为应激性生活事件的函数出现。