Objective: To determine the sensitivity and specificity of three depression screening scales to diagnose major depressive episodes in the elderly. Methods: Participants (n=129, 88% female) answered a semi-structured psychiatric interview (Mini International Neuropsychiatric Interview) to determine the diagnosis of major depressive disorder. After this, depressive symptoms in depressed and non-depressed subjects were assessed by independent administration of the 15-item Geriatric Depression Scale (GDS-15), Patient Health Questionnaire-9 (PHQ-9), and 17-item Hamilton Rating Scale for Depression . Results: Patients with major depression and controls did not differ in age and gender distribution. The sensitivity and specificity of all scales to identify a major depressive episode in older adults were X 90%. There were no significant differences between the areas under the curve for PHQ-9 vs. HDRS-17 (z = 1.2, p = 0.2), PHQ-9 vs. GDS-15 (z = 0.26, p = 0.8), or HDRS-17 vs. GDS-15 (z = 1.2, p = 0.2). Conclusion: This study provides evidence supporting the use of PHQ-9 and GDS-15, both of which are simple to administer and easy to interpret, to diagnose major depressive episodes in older adults without neurocognitive disorders.
These results highlight the importance of higher depressive symptoms, cognitive impairment and endocrine-metabolic disorders to the development of depressive symptoms in older adults. These findings provide a framework for the development of interventions to prevent the emergence of clinically significant depressive symptoms in the elderly.
Objective: A consistent body of research has confirmed that patients with major depressive disorder (MDD) have increased concentrations of pro-inflammatory cytokines, including IL-6, TNF-a, IL-1b, the soluble IL-2 receptor, and C-reactive protein, compared to controls; however, there is limited information on IL-17A in MDD. Moreover, information about IL-17A in older populations, i.e., patients with late-life depression (LLD), is conspicuously missing from the literature. The purpose of this study was to investigate the role of IL-17A in LLD. Methods: A convenience sample of 129 individuals, 74 with LLD and 55 non-depressed controls, were enrolled in this study. The Mann-Whitney U test was used to compare plasma IL-17A levels between LLD and controls subjects, and Spearman's rank order correlation was used to investigate correlation of these levels with clinical, neuropsychological, and cognitive assessments. Results: Plasma IL-17A levels were not statistically different between LLD patients and controls (p = 0.94). Among all subjects (LLD + control), plasma IL-17A did not correlate significantly with depressive symptoms (rho = -0.009, p = 0.92) but a significant correlation was observed with cognitive assessments (rho = 0.22, p = 0.01). Conclusion: Our findings do not support an association between plasma IL-17A levels and LLD. Nevertheless, IL-17A may be associated with cognitive impairment in LLD patients. If this finding is confirmed in future longitudinal studies, modulation of the T-helper 17 cell (T h 17) immune response may be a treatment target for cognitive impairment in this population.
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