Stress, Glucocorticoids, and Damage to the Nervous System: The Current State of Confusion.
Level 5 - mechanism / opinion, no new human data
Narrative review synthesizing mechanistic and preclinical literature without systematic search or original human data.
PubMed 9807058 · doi:10.3109/10253899609001092
What was done
Narrative review synthesizing literature on the deleterious effects of stress-induced glucocorticoids (GCs) on the brain, particularly the hippocampus. The paper outlines three phenotypic outcomes of GC exposure (atrophy, neurotoxicity, and neuroendangerment) and assesses five mechanistic themes underlying these actions.
What was found
The abstract reports no numerical data. It notes that GC actions include reversible dendritic atrophy following weeks of exposure, neuronal cell death following months of exposure, and neuroendangerment during acute insults such as stroke or seizure. It identifies five contributing mechanisms: metabolic vulnerability from inhibited glucose uptake, exacerbation of glutamate excess and calcium/oxygen radical cascades, impaired neuronal defenses, disrupted neurotrophin mobilization, and damaging electrophysiological alterations.
Why it matters
This review updates earlier models of stress-induced neurodegeneration by demonstrating that glucocorticoids damage neurons through multiple interacting cellular pathways beyond simple metabolic and energetic vulnerability.
Limits
As a narrative review, it lacks systematic search criteria, quality appraisal, and meta-analytic synthesis. No quantitative effect sizes or sample sizes are reported in the abstract, and the underlying evidence relies heavily on preclinical animal and in vitro models.
Cited by
- supports Low levels of cortisol are necessary for memory encoding, but high levels are toxic to the hippocampus.