Abstract
Background Late-onset depression is pathophysiologically distinct from early-onset depression, often requiring higher doses and a longer duration of antidepressant therapy to achieve a therapeutic response. Immune dysfunction, atherosclerosis, and vascular etiology are critical factors involved in the pathogenesis of late-onset depression. Based on this understanding, we hypothesize that levels of inflammatory markers in individuals with late-onset depression may be associated with their response to antidepressant therapy. Methodology Individuals aged >60 years who presented with their first depressive episode (as defined by the International Classification of Diseases, Tenth Revision, Diagnostic Criteria for Research) were recruited. A complete clinical assessment, C-reactive protein (CRP) level, and depression severity assessment using the Hamilton Depression Rating Scale (HAMD-17) were performed at baseline. Patients were prescribed antidepressant medication and reassessed for depression severity in HAMD after an eight-week follow-up. Results The study sample (n = 25) had a mean age of 64.7 ± 5.8 years and a baseline HAMD score of 18 ± 3. The overall response rate to antidepressant therapy was 24%. The mean age of individuals who responded to antidepressant therapy (n = 6) was 63.5 ± 4.9 years, and their baseline HAMD score was 16 ± 1.9. The mean age of individuals who were partial responders or non-responders to antidepressant therapy (n = 19) was 65.1 ± 6.1 years, and their baseline HAMD score was 18.5 ± 3.9. Additionally, there was a negative correlation between baseline CRP levels and antidepressant responsiveness (r = -0.6, p < 0.05). Conclusions Late-onset depression was less responsive to antidepressant medication, and a poor antidepressant response rate was associated with a higher level of CRP in late-onset depression.