To determine the frequency and correlates of impulse control disorders (ICDs) in Parkinson disease (PD).Design: An unstructured screening interview for ICDs (compulsive gambling, buying, and sexual behavior) followed by a telephone-administered structured interview for screen-positive patients.Setting: Two university-affiliated movement disorders centers.Participants: A convenience sample of 272 patients with idiopathic PD who were screened for psychiatric complications.Main Outcome Measures: Presence of compulsive gambling, buying, or sexual behavior as assessed by the Minnesota Impulsive Disorders Interview.

Frailty and depression are important issues affecting older adults. Depressive syndrome may be difficult to clinically disambiguate from frailty in advanced old age. Current reviews on the topic include studies with wide methodological variation. This review examined the published literature on cross-sectional and longitudinal associations between frailty and depressive symptomatology with either syndrome as the outcome, moderators of this relationship, construct overlap, and related medical and behavioral interventions. Prevalence of both was reported. A systematic review of studies published from 2000 to 2015 was conducted in PubMed, the Cochrane Database of Systematic Reviews, and PsychInfo. Key search terms were “frailty”, “frail”, “frail elderly”, “depressive”, “depressive disorder”, and “depression”. Participants of included studies were ≥55 years old and community dwelling. Included studies used an explicit biological definition of frailty based on Fried et al’s criteria and a screening measure to identify depressive symptomatology. Fourteen studies met the inclusion/exclusion criteria. The prevalence of depressive symptomatology, frailty, or their co-occurrence was greater than 10% in older adults ≥55 years old, and these rates varied widely, but less in large epidemiological studies of incident frailty. The prospective relationship between depressive symptomatology and increased risk of incident frailty was robust, while the opposite relationship was less conclusive. The presence of comorbidities that interact with depressive symptomatology increased incident frailty risk. Measurement variability of depressive symptomatology and inclusion of older adults who are severely depressed, have cognitive impairment or dementia, or stroke may confound the frailty syndrome with single disease outcomes, accounting for a substantial proportion of shared variance in the syndromes. Further study is needed to identify medical and behavioral interventions for frailty and depressive symptomatology that prevent adverse sequelae such as falls, disability, and premature mortality.

Objectives To examine the associations of depressive symptoms, antidepressant use, and duration of use with incident frailty three years later in nonfrail women ≥ age 65. Design Secondary analysis of the Women’s Health Initiative Observational Study (WHI-OS), a prospective cohort study. Setting WHI-OS was conducted in 40 U.S. clinical centers. Participants Women aged 65-79, not frail at baseline. Measurements Antidepressant use was assessed through medication container inspection at baseline. We created four groups according to baseline use and Burnam depression screen (range 0-1, 0.06 cut-off): antidepressant non-users without depressive symptoms (referent group), antidepressant non-users with depressive symptoms, antidepressant users without depressive symptoms, and antidepressant users with depressive symptoms. Frailty components included slowness/weakness, exhaustion, low physical activity, and unintended weight loss, ascertained through self-report and physical measurements at baseline and year 3. Results Among 27652 women at baseline, 4.9% (n=1350) were antidepressant users and 6.5% (n=1794) were categorized depressed. At year 3, 14.9% (n=4125) were frail. All groups had an increased risk for incident frailty compared to the referent group. Odds ratios ranged from 1.73 (95% Confidence Interval (CI) =1.41-2.12) among non-depressed antidepressant users to 3.63 among depressed antidepressant users (95% CI = 2.37-5.55). All durations of use were associated with incident frailty (<1 year OR = 1.95, 95% CI = 1.41-2.68; 1 to 3 years OR = 1.99, 95% CI = 1.45-2.74; > 3 years OR = 1.60, 95% CI = 1.20-2.14). Conclusion In older adult women, depressive symptoms and antidepressant use were associated with frailty after 3 years follow-up.

Background Genome-wide association studies (GWAS) have been unable to identify variants linked to depression. We hypothesized that examining depressive symptoms and considering gene-environment interaction (G×E) might improve efficiency for gene discovery. We therefore conducted a GWAS and genome-wide environment interaction study (GWEIS) of depressive symptoms. Methods Using data from the SHARe cohort of the Women’s Health Initiative, comprising African Americans (n=7179) and Hispanics/Latinas (n=3138), we examined genetic main effects and G×E with stressful life events and social support. We also conducted a heritability analysis using genome-wide complex trait analysis (GCTA). Replication was attempted in four independent cohorts. Results No SNPs achieved genome-wide significance for main effects in either discovery sample. The top signals in African Americans were rs73531535 (located 20kb from GPR139, p=5.75×10−8) and rs75407252 (intronic to CACNA2D3, p=6.99×10−7). In Hispanics/Latinas, the top signals were rs2532087 (located 27kb from CD38, p=2.44×10−7) and rs4542757 (intronic to DCC, p=7.31×10−7). In the GWEIS with stressful life events, one interaction signal was genome-wide significant in African Americans (rs4652467; p=4.10×10−10; located 14kb from CEP350). This interaction was not observed in a smaller replication cohort. Although heritability estimates for depressive symptoms and stressful life events were each less than 10%, they were strongly genetically correlated (rG=0.95), suggesting that common variation underlying depressive symptoms and stressful life event exposure, though modest on their own, were highly overlapping in this sample. Conclusions Our results underscore the need for larger samples, more GWEIS, and greater investigation into genetic and environmental determinants of depressive symptoms in minorities.

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