Thomas Alan J, Morris Christopher, Davis Sue, Jackson Elizabeth, Harrison Richard, O'Brien John T
School of Neurology, Neurobiology and Psychiatry, University of Newcastle upon Tyne, U.K.
Int Psychogeriatr. 2007 Oct;19(5):914-20. doi: 10.1017/S1041610206004728. Epub 2007 Jan 4.
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.
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-Asberg (MDRS) and Geriatric Depression (GDS) rating scales.
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.
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.
老年期抑郁症与血管疾病以及前额叶皮质中循环细胞因子和细胞黏附分子增加有关。我们假设，可溶性细胞间黏附分子-1（sICAM-1）和可溶性血管细胞黏附分子-1（sVCAM-1）在老年期重度抑郁症中会升高。
对60岁以上的重度抑郁症患者（N = 23）、亚综合征抑郁症患者（N = 20）和对照组（N = 25）测定血清sICAM-1和sVCAM-1水平。使用蒙哥马利-阿斯伯格抑郁量表（MDRS）和老年抑郁量表（GDS）评估抑郁严重程度。
抑郁症患者的sICAM-1（p = 0.240）或sVCAM-1（p = 0.600）没有显著升高，且这两种分子与抑郁严重程度均无相关性。校正认知障碍差异并未改变这些结果。早发性抑郁症患者（60岁之前）和晚发性抑郁症患者之间也没有差异。
这些发现并未提供证据表明先前报道的抑郁症患者血清细胞因子升高是由于外周血管疾病所致。尽管我们对受试者进行了血管疾病评估，但各组之间可能仍存在细微但重要的差异，这可能导致了我们的阴性结果。我们的结果表明，诸如与下丘脑-垂体-肾上腺（HPA）轴激活相关的中枢神经系统机制可能是抑郁症中炎症反应增强的原因。
