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Soluble cell adhesion molecules in late-life depression

Published online by Cambridge University Press:  04 January 2007

Alan J. Thomas
Affiliation:
School of Neurology, Neurobiology and Psychiatry, University of Newcastle upon Tyne, U.K. Institute for Ageing and Health, University of Newcastle upon Tyne, U.K. Older Persons Directorate, Gateshead Health NHS Trust, U.K.
Christopher Morris
Affiliation:
School of Neurology, Neurobiology and Psychiatry, University of Newcastle upon Tyne, U.K. Institute for Ageing and Health, University of Newcastle upon Tyne, U.K.
Sue Davis
Affiliation:
School of Neurology, Neurobiology and Psychiatry, University of Newcastle upon Tyne, U.K. Institute for Ageing and Health, University of Newcastle upon Tyne, U.K.
Elizabeth Jackson
Affiliation:
School of Neurology, Neurobiology and Psychiatry, University of Newcastle upon Tyne, U.K. Institute for Ageing and Health, University of Newcastle upon Tyne, U.K.
Richard Harrison
Affiliation:
Older Persons Directorate, Gateshead Health NHS Trust, U.K.
John T. O'Brien
Affiliation:
School of Neurology, Neurobiology and Psychiatry, University of Newcastle upon Tyne, U.K. Institute for Ageing and Health, University of Newcastle upon Tyne, U.K.

Abstract

Background: Late-life depression has been associated with vascular diseases and with increases in circulating cytokines and cell adhesion molecules in the prefrontal cortex. We hypothesized that soluble intercellular adhesion molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) would be increased in late-life major depression.

Methods: Serum levels of sICAM-1 and sVCAM-1 were measured in subjects over 60 with major depression (N = 23), subsyndromal depression (N = 20) and controls (N = 25). Depression severity was assessed using the Montgomery-Åsberg (MDRS) and Geriatric Depression (GDS) rating scales.

Results: There was no significant increase in sICAM-1 (p = 0.240) or sVCAM-1 (p = 0.600) in depression nor was there any correlation of either molecule with depression severity. Adjusting for differences in cognitive impairment did not alter these findings. There was also no difference between subjects with an early onset of depression (before 60) and those with late-onset depression.

Conclusions: These findings do not provide evidence that previously reported increases in serum cytokines in depression are due to peripheral vascular disease. Although we assessed subjects for vascular diseases it is possible that subtle but important differences between groups may still have been present and may have contributed to our negative findings.

Our results suggest central nervous system mechanisms, such as related to HPA axis activation, may be responsible for the enhanced inflammatory response in depression.

Type
Research Article
Copyright
International Psychogeriatric Association 2007

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