Evidence map›Paper›PMID 19317179›Full record

ReviewReviews in the neurosciences2008

Chronic stress-induced hippocampal vulnerability: the glucocorticoid vulnerability hypothesis.

Cheryl D Conrad

Open access · greenAbstract readReview
In one paragraph

Review in Reviews in the neurosciences, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
187citing papers in PubMed, 3 pooled it
5.2field-weighted citation impact, top 3% 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

187 citing papers in PubMed, 3 syntheses or guidelines pooled it, 412 citations in OpenAlex.

  1. Pooled it
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  7. Oxytocin as regulator of stress and inflammation in aging.Neuroscience and biobehavioral reviews · 2026
    Review
  8. Major depressive disorder-alcohol use disorder comorbidity: diagnosis, mechanisms and treatment.European archives of psychiatry and clinical neuroscience · 2026
    Review
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127 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

1 author at 1 institution in 1 country.

Cheryl D ConradArizona State University, Department of Psychology, Box 1104, Tempe, AZ 85282, USA. conradc@asu.edu
Arizona State University · US

Funding

Significance of Stress-Induced Hippocampal AtrophyR01MH064727 · NIMH · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI CONRAD, CHERYL D · 2002 to 2006
$1.0M
NIMH NIH HHS MH64727NIMH NIH HHS R01 MH064727
6 · The paper itself

Abstract

The hippocampus, a limbic structure important in learning and memory, is particularly sensitive to chronic stress and to glucocorticoids. While glucocorticoids are essential for an effective stress response, their oversecretion was originally hypothesized to contribute to age-related hippocampal degeneration. However, conflicting findings were reported on whether prolonged exposure to elevated glucocorticoids endangered the hippocampus and whether the primate hippocampus even responded to glucocorticoids as the rodent hippocampus did. This review discusses the seemingly inconsistent findings about the effects of elevated and prolonged glucocorticoids on hippocampal health and proposes that a chronic stress history, which includes repeated elevation of glucocorticoids, may make the hippocampus vulnerable to potential injury. Studies are described to show that chronic stress or prolonged exposure to glucocorticoids can compromise the hippocampus by producing dendritic retraction, a reversible form of plasticity that includes dendritic restructuring without irreversible cell death. Conditions that produce dendritic retraction are hypothesized to make the hippocampus vulnerable to neurotoxic or metabolic challenges. Of particular interest is the finding that the hippocampus can recover from dendritic retraction without any noticeable cell loss. When conditions surrounding dendritic retraction are present, the potential for harm is increased because dendritic retraction may persist for weeks, months or even years, thereby broadening the window of time during which the hippocampus is vulnerable to harm, called the 'glucocorticoid vulnerability hypothesis'. The relevance of these findings is discussed with regard to conditions exhibiting parallels in hippocampal plasticity, including Cushing's disease, major depressive disorder (MDD), and post-traumatic stress disorder (PTSD).

Indexed as

AnimalsGlucocorticoidsHippocampusHypothalamo-Hypophyseal SystemMajor Depressive DisorderPituitary-Adrenal SystemStress Disorders, Post-TraumaticStress, PsychologicalTime FactorsGlucocorticoids

Identifiers

PMID19317179
PMCPMC2746750
OpenAlexW2077552311

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.