Evidence map›Paper›PMID 20883718›Full record

ReviewNeuroscience and biobehavioral reviews2011

Depression: a repair response to stress-induced neuronal microdamage that can grade into a chronic neuroinflammatory condition?

Karen Wager-Smith, Athina Markou

Open access · greenAbstract readReview
In one paragraph

Review in Neuroscience and biobehavioral reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

59 citing papers in PubMed, 149 citations in OpenAlex.

  1. Trial
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  3. Glucose metabolism in the insula and cingulate is affected by systemic inflammation in humans.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2012
    Trial
  4. Review
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  10. Association between symptoms of psychological distress and cognitive functioning among adults with coronary artery disease.Stress and health : journal of the International Society for the Investigation of Stress · 2021
    Article
  11. Spontaneous Activity of CBFrontiers in pharmacology · 2021
    Article
  12. Article
  13. Article
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  15. Review
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  20. Inflammasome Activation by Methamphetamine Potentiates Lipopolysaccharide Stimulation of IL-1β Production in Microglia.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2018
    Article
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 1 institution in 1 country.

Karen Wager-SmithDepartment of Psychiatry, School of Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0603, USA. wagersmith@yahoo.com
Athina Markou
University of California, San Diego · US

Funding

Funct character of GABA_B receptor modulators, drug metabolism, pharmacokineticsU19DA026838 · NIDA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MARKOU, ATHINA · 2010 to 2014
$7.3M
Negative Symptoms of Schizophrenia: Animal ModelsR01MH062527 · NIMH · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MARKOU, ATHINA · 2002 to 2013
$3.5M
Gene Expression Profiling of Drug Addiction ModelsF32DA017403 · NIDA · SCRIPPS RESEARCH INSTITUTE · PI WAGER-SMITH, KAREN A · 2004 to 2004
$43k
NIDA NIH HHS 2U19DA026838NIDA NIH HHS F32 DA017403NIDA NIH HHS F32DA017403-01A1NIMH NIH HHS R01 MH062527
6 · The paper itself

Abstract

Depression is a major contributor to the global burden of disease and disability, yet it is poorly understood. Here we review data supporting a novel theoretical model for the biology of depression. In this model, a stressful life event leads to microdamage in the brain. This damage triggers an injury repair response consisting of a neuroinflammatory phase to clear cellular debris and a spontaneous tissue regeneration phase involving neurotrophins and neurogenesis. During healing, released inflammatory mediators trigger sickness behavior and psychological pain via mechanisms similar to those that produce physical pain during wound healing. The depression remits if the neuronal injury repair process resolves successfully. Importantly, however, the acute psychological pain and neuroinflammation often transition to chronicity and develop into pathological depressive states. This hypothesis for depression explains substantially more data than alternative models, including why emerging data show that analgesic, anti-inflammatory, pro-neurogenic and pro-neurotrophic treatments have antidepressant effects. Thus, an acute depressive episode can be conceptualized as a normally self-limiting but highly error-prone process of recuperation from stress-triggered neuronal microdamage.

Indexed as

AnimalsAntidepressive AgentsAnti-Inflammatory AgentsBrainDepressionEncephalitisHumansModels, BiologicalNeuronsPainStress, PsychologicalAntidepressive AgentsAnti-Inflammatory Agents

Identifiers

PMID20883718
PMCPMC3777427
OpenAlexW2051153602

What OpenQuestion holds

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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.