Prefrontal cortical deficits in type 1 diabetes mellitus: brain correlates of comorbid depression.
Prefrontal cortical deficits in type 1 diabetes mellitus: brain correlates of comorbid depression.
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DOI：
10.1001/archgenpsychiatry.2012.543
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发表时间：
2012-12
影响因子：
--
通讯作者：
Renshaw PF
中科院分区：
文献类型：
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作者：
Lyoo IK;Yoon S;Jacobson AM;Hwang J;Musen G;Kim JE;Simonson DC;Bae S;Bolo N;Kim DJ;Weinger K;Lee JH;Ryan CM;Renshaw PF
Neural substrates that may be responsible for the high prevalence of depression in type 1 diabetes mellitus (T1DM) have not yet been elucidated. To investigate neuroanatomic correlates of depression in T1DM. Case-control study using high-resolution brain magnetic resonance images. Joslin Diabetes Center and McLean Hospital, Massachusetts, and Seoul National University Hospital, South Korea. A total of 125 patients with T1DM (44 subjects with ≥1 previous depressive episodes [T1DM-depression group] and 81 subjects who had never experienced depressive episodes [T1DM-only group]), 23 subjects without T1DM but with 1 or more previous depressive episodes (depression group), and 38 healthy subjects (control group). Spatial distributions of cortical thickness for each diagnostic group were compared with the control group using a surface-based approach. Among patients with T1DM, associations between metabolic control measures and cortical thickness deficits were examined. Thickness reduction in the bilateral superior prefrontal cortical regions was observed in the T1DM-depression, T1DM-only, and depression groups relative to the control group at corrected P<.01. Conjunction analyses demonstrated that thickness reductions related to the influence of T1DM and those related to past depressive episode influence were observed primarily in the superior prefrontal cortical region. Long-term glycemic control levels were associated with superior prefrontal cortical deficits in patients with T1DM (β = −0.19, P = .02). This study provides evidence that thickness reduction of prefrontal cortical regions in patients with T1DM, as modified by long-term glycemic control, could contribute to the increased risk for comorbid depression.
