Objective:To test whether serum IL-1b is increased in late-life depression and whether any increase is related to depression severity.
Design:Comparison of serum IL-1b in 3 groups of elderly subjects (all >60) a) those with DSM-IV major depression who scored ³20 on the Montgomery-Asberg depression rating scale (MDRS), b) those with subsyndromal depression (previous major depression and currently scoring between 8 and 19 on the MDRS) and c) controls never had any psychiatric illness and scored <8 on the MDRS. Materials and Methods:Subjects gave informed consent to entering the study. None of the study subjects had evidence of dementia, neurological disorders or conditions normally regarded as inflammatory. No study subjects were taking oral steroids. All were assessed for cognitive impairment using the mini-mental state examination (MMSE) and the Cognitive Examination for the Elderly (the CAMCOG). Subjects scoring less than the standard cut-offs for global cognitive impairment (24 and 80 respectively) were excluded. The severity of depression was rated using both the MDRS and the 30 item Geriatric depression scale (GDS). A blood sample was taken for routine analysis and serum was aliquotted for ELISA. Human IL-1b was detected using a quantitative sandwich enzyme immunoassay (Amersham Biosciences UK Limited, U.K.). Subjects had a normal blood count, biochemistry and CRP. Groups were compared using unpaired t-tests and correlation coefficients were calculated to examine the relationship of depression severity to IL-1b levels.
Results:19 subjects with major depression, 20 subsyndromal depression and 21 controls met the entry criteria. There were no group differences in age, sex or CRP. The two depressed groups had significant cognitive impairment (MMSE, P<0.004; CAMCOG, P<0.001) compared with controls but not with each other (P>0.450). As expected the major depression group had more severe depression than the subsyndromal group (MDRS, P<0.001, GDS, P=0.017). Serum IL-1b was significantly increased in major depression compared with controls (P=0.003) but not compared with subsyndromal depression (P=0.166) who also did not differ from controls (P=0.131). Serum IL-1b was highly correlated with depression severity across the three groups (MDRS: r=0.443, P<0.001; GDS: r=0.396, P=0.004) but not with age or cognitive impairment (P>0.551).
Conclusion:These findings are consistent with the presence of an inflammatory response in late-life depression and indicate the severity of depression is associated with the degree of this response, suggesting it may be a state rather than a trait effect. The increase in IL-1b may be associated with abnormalities in the HPA axis, as with similar findings in younger adults, or with inflammation in prefrontal brain areas, as reported in our post mortem studies in late-life depression.
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