Evidence map›Paper›PMID 30715387›Full record

ArticleThe international journal of neuropsychopharmacology2019

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

Kei Itagaki, Minoru Takebayashi, Hiromi Abe, Chiyo Shibasaki, Naoto Kajitani, Mami Okada-Tsuchioka, Kotaro Hattori, Sumiko Yoshida, Hiroshi Kunugi, Shigeto Yamawaki

Open access · goldAbstract read
In one paragraph

Article in The international journal of neuropsychopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 20 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 1 country.

Kei ItagakiDivision of Psychiatry and Neuroscience, Institute for Clinical Research, NHO Kure Medical Center and Chugoku Cancer Center, Kure, Hiroshima, Japan.
Minoru TakebayashiDivision of Psychiatry and Neuroscience, Institute for Clinical Research, NHO Kure Medical Center and Chugoku Cancer Center, Kure, Hiroshima, Japan.
Hiromi AbeDivision of Psychiatry and Neuroscience, Institute for Clinical Research, NHO Kure Medical Center and Chugoku Cancer Center, Kure, Hiroshima, Japan.
Chiyo ShibasakiDivision of Psychiatry and Neuroscience, Institute for Clinical Research, NHO Kure Medical Center and Chugoku Cancer Center, Kure, Hiroshima, Japan.
Naoto KajitaniDivision of Psychiatry and Neuroscience, Institute for Clinical Research, NHO Kure Medical Center and Chugoku Cancer Center, Kure, Hiroshima, Japan.
Mami Okada-TsuchiokaDivision of Psychiatry and Neuroscience, Institute for Clinical Research, NHO Kure Medical Center and Chugoku Cancer Center, Kure, Hiroshima, Japan.
Kotaro HattoriDepartment of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan.
Sumiko YoshidaNational Center of Neurology and Psychiatry Hospital, Tokyo, Japan.
Hiroshi KunugiDepartment of Mental Disorder Research, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo, Japan.
Shigeto YamawakiMedical Genome Center, National Center of Neurology and Psychiatry, Tokyo, Japan.
Kure Medical Center · JPNational Center of Neurology and Psychiatry · JPKumamoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe 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.

methodsSerum 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.

resultsBefore 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).

conclusionThe 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.

Indexed as

Major Depressive DisorderAdultAgedElectroconvulsive TherapyFemaleHumansLysophospholipase DLysophospholipidsMaleMiddle AgedPhosphoric Diester Hydrolaseslysophosphatidic acidLysophospholipase DLysophospholipidsPhosphoric Diester Hydrolasesautotaxincerebrospinal fluidelectroconvulsive therapylysophosphatidic acidmajor depressive disorder

Identifiers

PMID30715387
PMCPMC6441130
OpenAlexW2912635869

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.