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Updated: Jul 17, 2026

Animal Models of Depression - Chronic Despair Model (CDM)
Published on: September 23, 2021
Soluble cell adhesion molecules in late-life depression.
Alan J Thomas1, Christopher Morris, Sue Davis
1School of Neurology, Neurobiology and Psychiatry, University of Newcastle upon Tyne, U.K. a.j.thomas@ncl.ac.uk
This study found no significant increase in soluble intercellular adhesion molecule-1 (sICAM-1) or soluble vascular cell adhesion molecule-1 (sVCAM-1) in late-life depression, suggesting other mechanisms may drive inflammation.
Area of Science:
- Neuroscience
- Psychiatry
- Immunology
Background:
- Late-life depression is linked to vascular issues and elevated cytokines.
- Increased cell adhesion molecules in the prefrontal cortex are observed in depression.
- Hypothesis: soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) are elevated in late-life major depression.
Purpose of the Study:
- To investigate serum levels of sICAM-1 and sVCAM-1 in older adults with major depression.
- To determine if these adhesion molecules correlate with depression severity.
- To explore the relationship between depression, vascular markers, and cognitive impairment.
Main Methods:
- Serum sICAM-1 and sVCAM-1 levels were measured in individuals over 60 with major depression, subsyndromal depression, and controls.
- Depression severity was assessed using the Montgomery-Asberg Depression Rating Scale (MDRS) and Geriatric Depression Scale (GDS).
- Analyses accounted for cognitive impairment and depression onset age.
Main Results:
- No significant increase in sICAM-1 or sVCAM-1 was found in depressed individuals compared to controls.
- No correlation was observed between sICAM-1 or sVCAM-1 levels and depression severity.
- Findings remained consistent after adjusting for cognitive impairment and comparing early- vs. late-onset depression.
Conclusions:
- The study does not support the hypothesis that increased serum cytokines in depression are solely due to peripheral vascular disease.
- Negative findings suggest that central nervous system mechanisms, potentially involving HPA axis activation, may underlie the inflammatory response in depression.
- While vascular diseases were assessed, subtle differences might still exist, warranting further investigation into neurobiological pathways.
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