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Reduced Serum and Cerebrospinal Fluid Levels of Autotaxin in Major Depressive Disorder.

Authors
  • Itagaki, Kei1, 2, 3
  • Takebayashi, Minoru1, 2, 4
  • Abe, Hiromi1
  • Shibasaki, Chiyo1, 3
  • Kajitani, Naoto1
  • Okada-Tsuchioka, Mami1
  • Hattori, Kotaro5, 6
  • Yoshida, Sumiko7
  • Kunugi, Hiroshi5
  • Yamawaki, Shigeto6
  • 1 Division of Psychiatry and Neuroscience, Institute for Clinical Research, NHO Kure Medical Center and Chugoku Cancer Center, Kure, Hiroshima, Japan. , (Japan)
  • 2 Department of Psychiatry, NHO Kure Medical Center and Chugoku Cancer Center, Kure, Hiroshima, Japan. , (Japan)
  • 3 Department of Psychiatry and Neurosciences, Division of Frontier Medical Science, Programs for Biomedical Research, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan. , (Japan)
  • 4 Department of Neuropsychiatry, Faculty of Life Sciences, Kumamoto University, Kumamoto, Japan. , (Japan)
  • 5 Department of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan. , (Japan)
  • 6 Medical Genome Center, National Center of Neurology and Psychiatry, Tokyo, Japan. , (Japan)
  • 7 National Center of Neurology and Psychiatry Hospital, Tokyo, Japan. , (Japan)
Type
Published Article
Journal
The International Journal of Neuropsychopharmacology
Publisher
Oxford University Press
Publication Date
Apr 01, 2019
Volume
22
Issue
4
Pages
261–269
Identifiers
DOI: 10.1093/ijnp/pyz005
PMID: 30715387
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

The autotaxin/lysophosphatidic acid axis is involved in diverse biological processes including neurodevelopment, inflammation, and immunological functioning. The lysophosphatidic acid 1 receptor has been implicated in the pathophysiology of major depressive disorder and in the mechanism of action of antidepressants. However, it is unclear whether central or peripheral autotaxin levels are altered in patients with major depressive disorder. Serum autotaxin levels were measured by an enzyme-linked immunosorbent assay in 37 patients with major depressive disorder diagnosed using DSM-IV-TR who underwent electroconvulsive therapy and were compared with those of 47 nondepressed controls matched for age and sex between January 2011 and December 2015. Patient serum levels of autotaxin before and after electroconvulsive therapy were also compared. In a separate sample set, cerebrospinal fluid autotaxin levels were compared between 26 patients with major depressive disorder and 27 nondepressed controls between December 2010 and December 2015. A potential association was examined between autotaxin levels and clinical symptoms assessed with the Hamilton Depression Rating Scale. Before electroconvulsive therapy, both serum and cerebrospinal fluidautotaxin levels were significantly lower in major depressive disorder patients than in controls (serum: P = .001, cerebrospinal fluid: P = .038). A significantly negative correlation between serum, but not cerebrospinal fluid, autotaxin levels and depressive symptoms was observed (P = .032). After electroconvulsive therapy, a parallel increase in serum autotaxin levels and depressive symptoms improvement was observed (P = .005). The current results suggest that serum autotaxin levels are reduced in a state-dependent manner. The reduction of cerebrospinal fluidautotaxin levels suggests a dysfunction in the autotaxin/lysophosphatidic acid axis in the brains of patients with major depressive disorder. © The Author(s) 2019. Published by Oxford University Press on behalf of CINP.

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