Evidence map›Paper›PMID 17707566›Full record

ReviewProgress in neuro-psychopharmacology & biological psychiatry2008

The neurobiology of retinoic acid in affective disorders.

J Douglas Bremner, Peter McCaffery

Open access · greenAbstract readReview
In one paragraph

Review in Progress in neuro-psychopharmacology & biological psychiatry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
72citing papers in PubMed, 1 pooled it
4.8field-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

72 citing papers in PubMed, 1 synthesis or guideline pooled it, 173 citations in OpenAlex.

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  15. Astrocytic RARγ mediates hippocampal astrocytosis and neurogenesis deficits in chronic retinoic acid-induced depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
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12 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.

J Douglas BremnerDepartment of Psychiatry, Emory University School of Medicine, Atlanta, GA 30306, USA. jdbremn@emory.edu
Peter McCaffery
Emory University · USUniversity of Aberdeen · GB

Funding

Neural Circuits in Women with Abuse and PTSDR01MH056120 · NIMH · YALE UNIVERSITY · PI BREMNER, JAMES DOUGLAS · 1999 to 2011
$5.0M
Mechanisms of Depression in CVDR01HL088726 · NHLBI · EMORY UNIVERSITY · PI BREMNER, JAMES DOUGLAS · 2008 to 2012
$2.6M
Biological Correlates of Traumatic StressK24MH076955 · NIMH · EMORY UNIVERSITY · PI BREMNER, JAMES DOUGLAS · 2006 to 2013
$946k
NHLBI NIH HHS R01 HL088726NIMH NIH HHS K24 MH076955NIMH NIH HHS R01 MH056120
6 · The paper itself

Abstract

Current models of affective disorders implicate alterations in norepinephrine, serotonin, dopamine, and CRF/cortisol; however treatments targeted at these neurotransmitters or hormones have led to imperfect resolution of symptoms, suggesting that the neurobiology of affective disorders is incompletely understood. Until now retinoids have not been considered as possible contributors to affective disorders. Retinoids represent a family of compounds derived from vitamin A that perform a large number of functions, many via the vitamin A product, retinoic acid. This signaling molecule binds to specific retinoic acid receptors in the brain which, like the glucocorticoid and thyroid hormone receptors, are part of the nuclear receptor superfamily and regulate gene transcription. Research in the field of retinoic acid in the CNS has focused on the developing brain, in part stimulated by the observation that isotretinoin (13-cis retinoic acid), an isomer of retinoic acid used in the treatment of acne, is highly teratogenic for the CNS. More recent work has suggested that retinoic acid may influence the adult brain; animal studies indicated that the administration of isotretinoin is associated with alterations in behavior as well as inhibition of neurogenesis in the hippocampus. Clinical evidence for an association between retinoids and depression includes case reports in the literature, studies of health care databases, and other sources. A preliminary PET study in human subjects showed that isotretinoin was associated with a decrease in orbitofrontal metabolism. Several studies have shown that the molecular components required for retinoic acid signaling are expressed in the adult brain; the overlap of brain areas implicated in retinoic acid function and stress and depression suggest that retinoids could play a role in affective disorders. This report reviews the evidence in this area and describes several systems that may be targets of retinoic acid and which contribute to the pathophysiology of depression.

Indexed as

AdultAnimalsBrainCorpus StriatumDisease Models, AnimalHippocampusHumansIsotretinoinMajor Depressive DisorderMiceMood DisordersNeurotransmitter AgentsPrefrontal CortexRetrospective StudiesSignal TransductionSuicideIsotretinoinNeurotransmitter AgentsTretinoin

Identifiers

PMID17707566
PMCPMC2704911
OpenAlexW2032840761

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.