Frontiers in Aging Neuroscience (Feb 2018)

Altered Connectivity of the Anterior Cingulate and the Posterior Superior Temporal Gyrus in a Longitudinal Study of Later-life Depression

  • Kenichiro Harada,
  • Toshikazu Ikuta,
  • Mami Nakashima,
  • Mami Nakashima,
  • Toshio Watanuki,
  • Masako Hirotsu,
  • Toshio Matsubara,
  • Toshio Matsubara,
  • Hirotaka Yamagata,
  • Yoshifumi Watanabe,
  • Koji Matsuo

DOI
https://doi.org/10.3389/fnagi.2018.00031
Journal volume & issue
Vol. 10

Abstract

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Patients with later-life depression (LLD) show abnormal gray matter (GM) volume, white matter (WM) integrity and functional connectivity in the anterior cingulate cortex (ACC) and posterior superior temporal gyrus (pSTG), but it remains unclear whether these abnormalities persist over time. We examined whether structural and functional abnormalities in these two regions are present within the same subjects during depressed vs. remitted phases. Sixteen patients with LLD and 30 healthy subjects were studied over a period of 1.5 years. Brain images obtained with a 3-Tesla magnetic resonance imaging (MRI) system were analyzed by voxel-based morphometry of the GM volume, and diffusion tensor imaging (DTI) and resting-state functional MRI were used to assess ACC–pSTG connectivity. Patients with LLD in the depressed and remitted phases showed significantly smaller GM volume in the left ACC and left pSTG than healthy subjects. Both patients with LLD in the depressed and remitted phases had significantly higher diffusivities in the WM tract of the left ACC–pSTG than healthy subjects. Remitted patients with LLD showed lower functional ACC–pSTG connectivity compared to healthy subjects. No difference was found in the two regions between depressed and remitted patients in GM volume, structural or functional connectivity. Functional ACC–pSTG connectivity was positively correlated with lower global function during remission. Our preliminary data show that structural and functional abnormalities of the ACC and pSTG occur during LLD remission. Our findings tentatively reveal the brain pathophysiology involved in LLD and may aid in developing neuroanatomical biomarkers for this condition.

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