TY - JOUR
T1 - Prefrontal cortical deficits in type 1 diabetes mellitus
T2 - Brain correlates of comorbid depression
AU - Lyoo, In Kyoon
AU - Yoon, Sujung
AU - Jacobson, Alan M.
AU - Hwang, Jaeuk
AU - Musen, Gail
AU - Kim, Jieun E.
AU - Simonson, Donald C.
AU - Bae, Sujin
AU - Bolo, Nicolas
AU - Kim, Dajung J.
AU - Weinger, Katie
AU - Lee, Junghyun H.
AU - Ryan, Christopher M.
AU - Renshaw, Perry F.
PY - 2012/12
Y1 - 2012/12
N2 - Context: Neural substrates that may be responsible for the high prevalence of depression in type 1 diabetes mellitus (T1DM) have not yet been elucidated. Objective: To investigate neuroanatomic correlates of depression in T1DM. Design: Case-control study using high-resolution brain magnetic resonance images. Settings: Joslin Diabetes Center and McLean Hospital, Massachusetts, and Seoul National University Hospital, South Korea. Participants: 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). Main Outcome Measures: 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. Results: 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). Conclusions: 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.
AB - Context: Neural substrates that may be responsible for the high prevalence of depression in type 1 diabetes mellitus (T1DM) have not yet been elucidated. Objective: To investigate neuroanatomic correlates of depression in T1DM. Design: Case-control study using high-resolution brain magnetic resonance images. Settings: Joslin Diabetes Center and McLean Hospital, Massachusetts, and Seoul National University Hospital, South Korea. Participants: 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). Main Outcome Measures: 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. Results: 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). Conclusions: 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.
UR - http://www.scopus.com/inward/record.url?scp=84870626646&partnerID=8YFLogxK
U2 - 10.1001/archgenpsychiatry.2012.543
DO - 10.1001/archgenpsychiatry.2012.543
M3 - Article
C2 - 23090665
AN - SCOPUS:84870626646
SN - 0003-990X
VL - 69
SP - 1267
EP - 1276
JO - Archives of General Psychiatry
JF - Archives of General Psychiatry
IS - 12
ER -