Evidence map›Paper›PMID 21918508›Full record

ReviewNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2012

Psychoneuroimmunology meets neuropsychopharmacology: translational implications of the impact of inflammation on behavior.

Ebrahim Haroon, Charles L Raison, Andrew H Miller

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 444 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
444citing papers in PubMed, 7 pooled it
–field-weighted citation impact
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

444 citing papers in PubMed, 7 syntheses or guidelines pooled it.

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384 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

3 authors.

Ebrahim HaroonDepartment of Psychiatry and Behavioral Sciences, Emory University School of Medicine, Atlanta, GA 30322, USA.
Charles L Raison
Andrew H Miller

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR025008 · NCRR · EMORY UNIVERSITY · PI STEPHENS, DAVID S · 2007 to 2011
$29.0M
Atlanta Clinical and Translational Science Institute (ACTSI) RenewalUL1TR000454 · NCATS · EMORY UNIVERSITY · PI STEPHENS, DAVID S · 2012 to 2016
$25.8M
X LINKED NYSTAGMUS SYNDROME WITH FEATURES OF ALBINISMM01RR000039 · NCRR · EMORY UNIVERSITY · PI BRANN, ALFRED W · 1985 to 2007
$21.3M
Mechanisms of MeditationR01AT004698 · NCCIH · UNIVERSITY OF ARIZONA · PI RAISON, CHARLES · 2009 to 2013
$3.1M
Phenotyping Major Depression with Increased InflammationR01MH087604 · NIMH · EMORY UNIVERSITY · PI MILLER, ANDREW H · 2010 to 2014
$2.2M
Dopaminergic Mechanisms of Cytokine-Induced Behavioral ChangeR01MH083746 · NIMH · EMORY UNIVERSITY · PI MILLER, ANDREW H · 2009 to 2012
$1.5M
Neuroimmune Mechanisms of Glucocorticoid ResistanceR01MH075102 · NIMH · EMORY UNIVERSITY · PI MILLER, ANDREW H · 2006 to 2010
$1.0M
MR SPECTROSCOPY TO REVEAL CNS MECHANISMS OF CYTOKINE-INDUCED BEHAVIORAL CHANGEK23MH091254 · NIMH · EMORY UNIVERSITY · PI HAROON, EBRAHIM · 2010 to 2014
$883k
NCATS NIH HHS UL1 TR000454NCCIH NIH HHS R01 AT004698NCCIH NIH HHS R01AT004698NCRR NIH HHS M01 RR000039NCRR NIH HHS M01 RR0039NCRR NIH HHS UL1 RR025008NIMH NIH HHS K23 MH091254NIMH NIH HHS K23MH091254NIMH NIH HHS R01 MH075102NIMH NIH HHS R01MH075102NIMH NIH HHS R01 MH083746NIMH NIH HHS R01MH083746NIMH NIH HHS R01 MH087604NIMH NIH HHS R01MH087604NIMH NIH HHS R01MH75102
6 · The paper itself

Abstract

The potential contribution of chronic inflammation to the development of neuropsychiatric disorders such as major depression has received increasing attention. Elevated biomarkers of inflammation, including inflammatory cytokines and acute-phase proteins, have been found in depressed patients, and administration of inflammatory stimuli has been associated with the development of depressive symptoms. Data also have demonstrated that inflammatory cytokines can interact with multiple pathways known to be involved in the development of depression, including monoamine metabolism, neuroendocrine function, synaptic plasticity, and neurocircuits relevant to mood regulation. Further understanding of mechanisms by which cytokines alter behavior have revealed a host of pharmacologic targets that may be unique to the impact of inflammation on behavior and may be especially relevant to the treatment and prevention of depression in patients with evidence of increased inflammation. Such targets include the inflammatory signaling pathways cyclooxygenase, p38 mitogen-activated protein kinase, and nuclear factor-κB, as well as the metabolic enzyme, indoleamine-2,3-dioxygenase, which breaks down tryptophan into kynurenine. Other targets include the cytokines themselves in addition to chemokines, which attract inflammatory cells from the periphery to the brain. Psychosocial stress, diet, obesity, a leaky gut, and an imbalance between regulatory and pro-inflammatory T cells also contribute to inflammation and may serve as a focus for preventative strategies relevant to both the development of depression and its recurrence. Taken together, identification of mechanisms by which cytokines influence behavior may reveal a panoply of personalized treatment options that target the unique contributions of the immune system to depression.

Indexed as

AnimalsHumansInflammationMental DisordersNeuropharmacologyPsychoneuroimmunologyPsychopharmacology

Identifiers

PMID21918508
PMCPMC3238082

What OpenQuestion holds

Textmetadata
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.