Neural state and trait bases of mood-incongruent memory formation and retrieval in first-episode major depression
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- 作者：Guido A. van Wingen ; Philip van Eijndhoven ; Henk R. Cremers ; Indira Tendolkar ; Robbert Jan Verkes ; Jan K. Buitelaar ; Guillé ; n Ferná ; ndez
- 关键词：MDD ; fMRI ; Memory ; Emotion ; Faces ; Amygdala
- 刊名：Journal of Psychiatric Research
- 出版年：2010
- 出版时间：June 2010
- 年：2010
- 卷：44
- 期：8
- 页码：527-534
- 全文大小：320 K
文摘
Mood-congruent cognitive biases constitute critical factors for the vulnerability to depression and its maintenance. One important aspect is impaired memory for positive information during depression and after recovery. To elucidate its state (during depression only) and trait (during depression and recovery) related neural bases, we investigated medication free depressed, recovered, and healthy individuals with functional MRI while they memorized and recognized happy and neutral face stimuli. The imaging results revealed group differences in mood-incongruent successful memory encoding and retrieval activity already in the absence of significant memory performance differences. State effects were observed in the amygdala and posterior cingulate cortex. Whereas the amygdala was generally involved in memory formation, its activity predicted subsequent forgetting of neutral faces in depressed patients. Furthermore, the amygdala and posterior cingulate cortex were involved in memory retrieval of happy faces in depressed patients only. Trait effects were observed in the fusiform gyrus and prefrontal cortex. The fusiform gyrus was involved in memory formation and retrieval of happy faces in both patient groups, whereas it was involved in memory formation and retrieval of neutral faces in healthy individuals. Similar trait effects were observed during memory retrieval in the orbitofrontal cortex and left inferior frontal gyrus. Thus, while memory processing of positive information in the amygdala and posterior cingulate cortex is biased during depression only, memory processing in the fusiform gyrus and prefrontal cortex is biased also after recovery. These distinct neural mechanisms may respectively constitute symptom maintenance and cognitive vulnerability factors for depression.