Soluble cell adhesion molecules in late-life depression

被引:19
作者
Thomas, Alan J.
Morris, Christopher
Davis, Sue
Jackson, Elizabeth
Harrison, Richard
O'Brien, John T.
机构
[1] Newcastle Univ, Sch Neurol Neurobiol & Psychiat, Newcastle Upon Tyne, Tyne & Wear, England
[2] Newcastle Univ, Inst Ageing & Hlth, Newcastle Upon Tyne, Tyne & Wear, England
基金
英国医学研究理事会;
关键词
major depression; inflammation; vascular disease; cytokines;
D O I
10.1017/S1041610206004728
中图分类号
B849 [应用心理学];
学科分类号
040203 ;
摘要
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-angstrom serg (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.
引用
收藏
页码:914 / 920
页数:7
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