Postmortem studies in mood disorders indicate altered numbers of neurons and glial cells
Abstract
The influence of stress and glucocorticoids on neuronal pathology has been demonstrated in animal and clinical studies. It has been proposed that stress-induced changes in the hippocampus may be central to the development of depression in genetically vulnerable individuals. New evidence implicates the prefrontal cortex (PFC) in addition to the hippocampus as a site of neuropathology in depression. The PFC may be involved in stress-mediated neurotoxicity because stress alters PFC functions and glucocorticoid receptors, the PFC is directly interconnected with the hippocampus, and metabolic alterations are present in the PFC in depressed patients. Postmortem studies in major depression and bipolar disorder provide the first evidence for specific neuronal and glial histopathology in mood disorders. Three patterns of morphometric cellular changes are noted: cell loss (subgenual PFC), cell atrophy (dorsolateral PFC and orbitofrontal cortex), and increased numbers of cells (hypothalamus, dorsal raphe nucleus). The relevance of cellular changes in mood disorders to stress and prolonged PFC development and a role of neurotrophic/neuroprotective factors are suggested, and a link between cellular changes and the action of therapeutic drugs is discussed. The precise anatomic localization of dysfunctional neurons and glia in mood disorders may reveal cortical targets for novel antidepressants and mood stabilizers.
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Postmortem studies of MDD cases show deficits in neuroglial numbers in the neocortex.
“Postmortem studies of MDD cases show deficits in neuroglial numbers in the neocortex.268”
From Epigenetic regulation in major depression and other stress-related disorders: molecular mechanisms, clinical relevance and therapeutic potential (2023) · cites this paper as [268]
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- Authors
- Rajkowska, G.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2000-10
- Volume
- 48
- Issue
- 8
- Pages
- 766-777
- ISSN
- 0006-3223 (ISSN-L)
- OpenAlex
- W2087955490
- Cited by
- 822
- References
- 8
- Citations by year
- 2026: 7 · 2025: 12 · 2024: 14 · 2023: 15 · 2022: 20 · 2021: 49 · 2020: 17 · 2019: 28 · 2018: 24 · 2017: 27 · 2016: 40 · 2015: 30 · 2014: 44 · 2013: 30 · 2012: 34
- FWCI
- 28.24
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- U.S. Public Health Service (55872)
- Topics
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- mood disorders, major depressive disorder, bipolar disorder, postmortem brain, glial cells, prefrontal cortex, hippocampus, stress, glucocorticoids, glucocorticoid receptor, neurotoxicity, subgenual prefrontal cortex, dorsolateral prefrontal cortex, orbitofrontal cortex, hypothalamus, dorsal raphe nucleus, cell loss, neurotrophic factors, antidepressants, mood stabilizers
- MeSH terms
- Atrophy, Glial Fibrillary Acidic Protein, Humans, Neuroglia, Neurons, Stress, Psychological, Brain-Derived Neurotrophic Factor, Mood Disorders
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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