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Background: Little is known about patterns of depression symptoms over time in older adults. This study aims to assess the association of childhood maltreatment and cortisol levels with latent classes of depression symptoms over ten years in older adults. Methods: A total of 752 participants (mean age 61.7±9.5, female 18%) in the Second Manifestations of ARTerial disease-Memory, depression and aging (SMART-Medea) study provided up to twenty measures of depression symptoms over ten years based on the Patient Health Questionnaire-9 (PHQ-9). At baseline, salivary cortisol was measured, and childhood maltreatment was assessed. Responses to the PHQ-9 were indicators in a latent class analysis. Multinomial regression determined associations between class membership and cortisol and maltreatment, adjusting for age, sex, and education. Results: Four distinct classes were identified; never depressed (n=275, 37%), energy/sleep difficulties (n=237, 32%), mild depression symptoms (n=152, 20%) and fluctuating severe depression (n=88, 12%). Childhood maltreatment was associated with mild depression symptoms (OR=1.95, 95% CI: 1.17-3.25) and fluctuating severe depression (OR=3.50, 95% CI: 1.99-6.15). Blunted morning cortisol was associated with energy/sleep difficulties (OR=0.98, 95% CI: 0.95-1.00) and fluctuating severe depression (OR=0.96, 95% CI: 0.92-0.99). There was no evidence for interaction between maltreatment and cortisol.Limitations: There is limited generalizability due to the cohort consisting of participants with atherosclerosis and being mostly male. This study utilizes retrospective self-reporting of childhood maltreatment. Conclusion: Childhood maltreatment and blunted morning cortisol independently contribute to a worse depression course. Blunted morning cortisol may contribute to sub-clinical depression symptoms, specifically difficulties with energy levels and sleep.

24 december 2022, Item does not contain fulltext, Clinical populations with basal ganglia pathologies may present with language production impairments, which are often described in combination with comprehension measures or attributed to motor, memory, or processing-speed problems. In this systematic review and meta-analysis, we studied word production in four (vascular and non-vascular) pathologies of the basal ganglia: stroke affecting the basal ganglia, small vessel disease, Parkinson's disease, and Huntington's disease. We compared scores of these clinical populations with those of matched cognitively unimpaired adults on four well-established production tasks, namely picture naming, category fluency, letter fluency, and past-tense verb inflection. We conducted a systematic search in PubMed and PsycINFO with terms for basal ganglia structures, basal ganglia disorders and language production tasks. A total of 114 studies were included, containing results for one or more of the tasks of interest. For each pathology and task combination, effect sizes (Hedges' g) were extracted comparing patient versus control groups. For all four populations, performance was consistently worse than that of cognitively unimpaired adults across the four language production tasks (p-values < 0.010). Given that performance in picture naming and verb inflection across all pathologies was quantified in terms of accuracy, our results suggest that production impairments cannot be fully explained by motor or processing-speed deficits. Our review shows that while language production difficulties in these clinical populations are not negligible, more evidence is necessary to determine the exact mechanism that leads to these deficits and whether this mechanism is the same across different pathologies.