Evidence map›Paper›PMID 27824355›Full record

ReviewTranslational psychiatry2016

Neuropathology of mood disorders: do we see the stigmata of inflammation?

N Mechawar, J Savitz

Open access · goldAbstract readReview
In one paragraph

Review in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
102citing papers in PubMed, 4 pooled it
10.7field-weighted citation impact, top 1% 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

102 citing papers in PubMed, 4 syntheses or guidelines pooled it, 164 citations in OpenAlex.

  1. Pooled it
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  4. A Specific Inflammatory Profile Underlying Suicide Risk? Systematic Review of the Main Literature Findings.International journal of environmental research and public health · 2020
    Pooled it
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42 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 2 countries.

N MechawarDouglas Mental Health University Institute and Department of Psychiatry, McGill University, Montreal, QC, Canada.
J SavitzLaureate Institute for Brain Research, Tulsa, OK, USA.
Douglas Mental Health University Institute · CAUniversity of Tulsa · US

Funding

Neuroimaging abnormalities in major depressive disorder: effect of inflammationK01MH096077 · NIMH · LAUREATE INSTITUTE FOR BRAIN RESEARCH · PI SAVITZ, JONATHAN · 2012 to 2016
$906k
CIHRNIMH NIH HHS K01 MH096077
6 · The paper itself

Abstract

A proportion of cases with mood disorders have elevated inflammatory markers in the blood that conceivably may result from stress, infection and/or autoimmunity. However, it is not yet clear whether depression is a neuroinflammatory disease. Multiple histopathological and molecular abnormalities have been found postmortem but the etiology of these abnormalities is unknown. Here, we take an immunological perspective of this literature. Increases in activated microglia or perivascular macrophages in suicide victims have been reported in the parenchyma. In contrast, astrocytic markers generally are downregulated in mood disorders. Impairment of astrocytic function likely compromises the reuptake of glutamate potentially leading to excitotoxicity. Inflammatory cytokines and microglia/macrophage-derived quinolinic acid (QA) downregulate the excitatory amino acid transporters responsible for this reuptake, while QA has the additional effect of inhibiting astroglial glutamine synthetase, which converts glutamate to glutamine. Given that oligodendroglia are particularly vulnerable to inflammation, it is noteworthy that reductions in numbers or density of oligodendrocyte cells are one of the most prominent findings in depression. Structural and/or functional changes to GABAergic interneurons also are salient in postmortem brain samples, and may conceivably be related to early inflammatory insults. Although the postmortem data are consistent with a neuroimmune etiology in a subgroup of depressed individuals, we do not argue that all depression-associated abnormalities are reflective of a neuroinflammatory process or even that all immunological activity in the brain is deleterious. Rather, we highlight the pervasive role of immune signaling pathways in brain function and provide an alternative perspective on the current postmortem literature.

Indexed as

AstrocytesAutoimmune Diseases of the Nervous SystemBipolar DisorderBraingamma-Aminobutyric AcidHumansInflammationInflammation MediatorsInterneuronsMajor Depressive DisorderMicrogliaNeuronsOligodendrogliaStress, PsychologicalSuicidegamma-Aminobutyric AcidInflammation Mediators

Identifiers

PMID27824355
PMCPMC5314124
OpenAlexW2556540841

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.