Anxiety is a common comorbid feature of late-life depression (LLD) and is associated with poorer global cognitive functioning independent of depression severity. However, little is known about whether comorbid anxiety is associated with a domain-specific pattern of cognitive dysfunction. We therefore examined group differences (LLD with and without comorbid anxiety) in cognitive functioning performance across multiple domains.

Older adults with major depressive disorder (N = 228, ages 65–91) were evaluated for anxiety and depression severity, and cognitive functioning (learning, memory, language, processing speed, executive functioning, working memory, and visuospatial functioning). Ordinary least squares regression adjusting for age, sex, education, and concurrent depression severity examined anxiety group differences in performance on tests of cognitive functioning.

Significant group differences emerged for confrontation naming and visuospatial functioning, as well as for verbal fluency, working memory, and inhibition with lower performance for LLD with comorbid anxiety compared to LLD only, controlling for depression severity.

Performance patterns identified among older adults with LLD and comorbid anxiety resemble neuropsychological profiles typically seen in neurodegenerative diseases of aging. These findings have potential implications for etiological considerations in the interpretation of neuropsychological profiles.

Late-life depression (LLD) is common and frequently co-occurs with neurodegenerative diseases of aging. Little is known about how heterogeneity within LLD relates to factors typically associated with neurodegeneration. Varying levels of anxiety are one source of heterogeneity in LLD. We examined associations between anxiety symptom severity and factors associated with neurodegeneration, including regional brain volumes, amyloid beta (Aβ) deposition, white matter disease, cognitive dysfunction, and functional ability in LLD.

Older adults with major depression (N = 121, Ages 65–91) were evaluated for anxiety severity and the following: brain volume (orbitofrontal cortex [OFC], insula), cortical Aβ standardized uptake value ratio (SUVR), white matter hyperintensity (WMH) volume, global cognition, and functional ability. Separate linear regression analyses adjusting for age, sex, and concurrent depression severity were conducted to examine associations between anxiety and each of these factors. A global regression analysis was then conducted to examine the relative associations of these variables with anxiety severity.

Greater anxiety severity was associated with lower OFC volume (β = −68.25, t = −2.18, p = .031) and greater cognitive dysfunction (β = 0.23, t = 2.46, p = .016). Anxiety severity was not associated with insula volume, Aβ SUVR, WMH, or functional ability. When examining the relative associations of cognitive functioning and OFC volume with anxiety in a global model, cognitive dysfunction (β = 0.24, t = 2.62, p = .010), but not OFC volume, remained significantly associated with anxiety.

Among multiple factors typically associated with neurodegeneration, cognitive dysfunction stands out as a key factor associated with anxiety severity in LLD which has implications for cognitive and psychiatric interventions.

Perceived cognitive dysfunction is a common feature of late-life depression (LLD) that is associated with diminished quality of life and greater disability. Similar associations have been demonstrated in individuals with Hoarding Disorder. The degree to which hoarding behaviors (HB) are associated with greater perceived cognitive dysfunction and disability in individuals with concurrent LLD is not known.

Participants with LLD (N=83) completed measures of hoarding symptom severity (Savings Inventory-Revised; SI-R) and were classified into two groups based on HB severity: LLD+HB who exhibited significant HB (SI-R . 41, n = 25) and LLD with low HB (SI-R < 41, n = 58). Additional measures assessed depression severity (Hamilton Depression Rating Scale; HDRS), perceived cognitive difficulties (Everyday Cognition Scale; ECOG), and disability (World Health Organization Disability Assessment Scale [WHODAS]-II-Short). Given a non-normal distribution of ECOG and WHODAS-II scores, non-parametric Wilcoxon-Mann-Whitney tests were used to assess group differences in perceived cognitive dysfunction and disability. A regression model assessed the extent to which perceived cognitive dysfunction was associated with hoarding symptom severity measured continuously, covarying for age, education, gender, and depression severity. A separate regression model assessed the extent to which disability scores were associated with perceived cognitive dysfunction and HB severity covarying for demographics and depression severity.

LLD+HB endorsed significantly greater perceived cognitive dysfunction (W = 1023, p = 0.003) and greater disability (W = 1006, p = < 0.001) compared to LLD. Regression models accounting for demographic characteristics and depression severity revealed that greater HB severity was associated with greater perceived cognitive dysfunction (β = 0.009, t = 2.765, p = 0.007). Increased disability was associated with greater perceived cognitive dysfunction (β = 4.792, t(71) = 3.551, p = 0.0007) and HB severity (β = 0.080, t(71) = 1.944, p = 0.056) approached significance after accounting for variance explained by depression severity and demographic covariates.

Our results suggest that hoarding behaviors are associated with increased perceived cognitive dysfunction and greater disability in individuals with LLD. Screening for HB in individuals with LLD may help identify those at greater risk for poor cognitive and functional outcomes. Interventions that target HB and perceived cognitive difficulties may decrease risk for disability in LLD. However, longitudinal studies would be required to further evaluate these relationships.

Late Life Major Depressive Disorder (LLD) and Hoarding Disorder (HD) are common in older adults with prevalence estimates up to 29% and 7%, respectively. Both LLD and HD are characterized by executive dysfunction and disability. There is evidence of overlapping neurobiological dysfunction in LLD and HD suggesting potential for compounded executive dysfunction and disability in the context of comorbid HD and LLD. Yet, prevalence of HD in primary presenting LLD has not been examined and potential compounded impact on executive functioning, disability, and treatment response remains unknown. Thus, the present study aimed to determine the prevalence of co-occurring HD in primary presenting LLD and examine hoarding symptom severity as a contributor to executive dysfunction, disability, and response to treatment for LLD.

Eighty-three adults ages 65-90 participating in a psychotherapy study for LLD completed measures of hoarding symptom severity (Savings Inventory-Revised: SI-R), executive functioning (WAIS-IV Digit Span, Letter-Number Sequencing, Coding; Stroop Interference; Trail Making Test-Part B; Letter Fluency), functional ability (World Health Organization Disability Assessment Schedule-II-Short), and depression severity (Hamilton Depression Rating Scale) at post-treatment. Pearson's Chi-squared tests evaluated group differences in cognitive and functional impairment rates and depression treatment response between participants with (HD+LLD) and without (LLD-only) clinically significant hoarding symptoms. Linear regressions were used to examine the association between hoarding symptom severity and executive function performance and functional ability and included as covariates participant age, years of education, gender, and concurrent depression severity.

At post-treatment, 24.1% (20/83) of participants with LLD met criteria for clinically significant hoarding symptoms (SI-R.41). Relative to LLD-only, the LLD+HD group demonstrated greater impairment rates in Letter-Number Sequencing (χ2(1)=4.0, p=.045) and Stroop Interference (χ2(1)=4.8, p=.028). Greater hoarding symptom severity was associated with poorer executive functioning performance on Digit Span (t(71)=-2.4, β=-0.07, p=.019), Letter-Number Sequencing (t(70)=-2.1, β=-0.05, p=.044), and Letter Fluency (t(71)=-2.8, β=-0.24, p=.006). Rates of functional impairment were significantly higher in the LLD+HD (88.0%) group compared to the LLD-only (62.3%) group, (χ2(1)=5.41, p=.020). Additionally, higher hoarding symptom severity was related to greater disability (t(72)=2.97, β=0.13, p=.004). Furthermore, depression treatment response rates were significantly lower in the LLD+HD group at 24.0% (6/25) compared to 48.3% (28/58) in the LLD-only group, χ2(1)=4.26, p=.039.

The present study is among the first to report prevalence of clinically significant hoarding symptoms in primary presenting LLD. The findings of 24.1% co-occurrence of HD in primary presenting LLD and increased burden on executive functioning, disability, and depression treatment outcomes have important implications for intervention and prevention efforts. Hoarding symptoms are likely under-evaluated, and thus may be overlooked, in clinical settings where LLD is identified as the primary diagnosis. Taken together with results indicating poorer depression treatment response in LLD+HD, these findings underscore the need for increased screening of hoarding behaviors in LLD and tailored interventions for this LLD+HD group. Future work examining the course of hoarding symptomatology in LLD (e.g., onset age of hoarding behaviors) may provide insights into the mechanisms associated with greater executive dysfunction and disability.

To describe the cumulative seroprevalence of severe acute respiratory coronavirus virus 2 (SARS-CoV-2) antibodies during the coronavirus disease 2019 (COVID-19) pandemic among employees of a large pediatric healthcare system.

Prospective observational cohort study open to adult employees at the Children’s Hospital of Philadelphia, conducted April 20–December 17, 2020.

Employees were recruited starting with high-risk exposure groups, utilizing e-mails, flyers, and announcements at virtual town hall meetings. At baseline, 1 month, 2 months, and 6 months, participants reported occupational and community exposures and gave a blood sample for SARS-CoV-2 antibody measurement by enzyme-linked immunosorbent assays (ELISAs). A post hoc Cox proportional hazards regression model was performed to identify factors associated with increased risk for seropositivity.

In total, 1,740 employees were enrolled. At 6 months, the cumulative seroprevalence was 5.3%, which was below estimated community point seroprevalence. Seroprevalence was 5.8% among employees who provided direct care and was 3.4% among employees who did not perform direct patient care. Most participants who were seropositive at baseline remained positive at follow-up assessments. In a post hoc analysis, direct patient care (hazard ratio [HR], 1.95; 95% confidence interval [CI], 1.03–3.68), Black race (HR, 2.70; 95% CI, 1.24–5.87), and exposure to a confirmed case in a nonhealthcare setting (HR, 4.32; 95% CI, 2.71–6.88) were associated with statistically significant increased risk for seropositivity.

Employee SARS-CoV-2 seroprevalence rates remained below the point-prevalence rates of the surrounding community. Provision of direct patient care, Black race, and exposure to a confirmed case in a nonhealthcare setting conferred increased risk. These data can inform occupational protection measures to maximize protection of employees within the workplace during future COVID-19 waves or other epidemics.

Studying phenotypic and genetic characteristics of age at onset (AAO) and polarity at onset (PAO) in bipolar disorder can provide new insights into disease pathology and facilitate the development of screening tools.

To examine the genetic architecture of AAO and PAO and their association with bipolar disorder disease characteristics.

Genome-wide association studies (GWASs) and polygenic score (PGS) analyses of AAO (n = 12 977) and PAO (n = 6773) were conducted in patients with bipolar disorder from 34 cohorts and a replication sample (n = 2237). The association of onset with disease characteristics was investigated in two of these cohorts.

Earlier AAO was associated with a higher probability of psychotic symptoms, suicidality, lower educational attainment, not living together and fewer episodes. Depressive onset correlated with suicidality and manic onset correlated with delusions and manic episodes. Systematic differences in AAO between cohorts and continents of origin were observed. This was also reflected in single-nucleotide variant-based heritability estimates, with higher heritabilities for stricter onset definitions. Increased PGS for autism spectrum disorder (β = −0.34 years, s.e. = 0.08), major depression (β = −0.34 years, s.e. = 0.08), schizophrenia (β = −0.39 years, s.e. = 0.08), and educational attainment (β = −0.31 years, s.e. = 0.08) were associated with an earlier AAO. The AAO GWAS identified one significant locus, but this finding did not replicate. Neither GWAS nor PGS analyses yielded significant associations with PAO.

AAO and PAO are associated with indicators of bipolar disorder severity. Individuals with an earlier onset show an increased polygenic liability for a broad spectrum of psychiatric traits. Systematic differences in AAO across cohorts, continents and phenotype definitions introduce significant heterogeneity, affecting analyses.

Black, Asian and minority ethnicity groups may experience better health outcomes when living in areas of high own-group ethnic density – the so-called ‘ethnic density’ hypothesis. We tested this hypothesis for the treatment outcome of compulsory admission.

Data from the 2010–2011 Mental Health Minimum Dataset (N = 1 053 617) was linked to the 2011 Census and 2010 Index of Multiple Deprivation. Own-group ethnic density was calculated by dividing the number of residents per ethnic group for each lower layer super output area (LSOA) in the Census by the LSOA total population. Multilevel modelling estimated the effect of own-group ethnic density on the risk of compulsory admission by ethnic group (White British, White other, Black, Asian and mixed), accounting for patient characteristics (age and gender), area-level deprivation and population density.

Asian and White British patients experienced a reduced risk of compulsory admission when living in the areas of high own-group ethnic density [odds ratios (OR) 0.97, 95% credible interval (CI) 0.95–0.99 and 0.94, 95% CI 0.93–0.95, respectively], whereas White minority patients were at increased risk when living in neighbourhoods of higher own-group ethnic concentration (OR 1.18, 95% CI 1.11–1.26). Higher levels of own-group ethnic density were associated with an increased risk of compulsory admission for mixed-ethnicity patients, but only when deprivation and population density were excluded from the model. Neighbourhood-level concentration of own-group ethnicity for Black patients did not influence the risk of compulsory admission.

We found only minimal support for the ethnic density hypothesis for the treatment outcome of compulsory admission to under the Mental Health Act.