Should COVID-19 have a direct impact on the risk of depression, it would suggest specific pathways for prevention and treatment. In this retrospective population-based study, we aimed to examine the association of prior SARS-CoV-2 infection with depressive symptoms, distinguishing self-reported v. biologically confirmed COVID-19.

32 007 participants from the SAPRIS survey nested in the French CONSTANCES cohort were included. COVID-19 was measured as followed: ad hoc serologic testing, self-reported PCR or serology positive test results, and self-reported COVID-19. Depressive symptoms were measured with the Center of Epidemiologic Studies-Depression Scale (CES-D). Outcomes were depressive symptoms (total CES-D score, its four dimensions, and clinically significant depressive symptoms) and exposure was prior COVID-19 (no COVID-19/self-reported unconfirmed COVID-19/biologically confirmed COVID-19).

In comparison to participants without COVID-19, participants with self-reported unconfirmed COVID-19 and biologically confirmed COVID-19 had higher CES-D scores (β for one interquartile range increase [95% CI]: 0.15 [0.08–0.22] and 0.09 [0.05–0.13], respectively) and somatic complaints dimension scores (0.15 [0.09–0.21] and 0.10 [0.07–0.13]). Only those with self-reported but unconfirmed COVID-19 had higher depressed affect dimension scores (0.08 [0.01–0.14]). Accounting for ad hoc serologic testing only, the CES-D score and the somatic complaints dimension were only associated with the combination of self-reported COVID-19 and negative serology test results.

The association between COVID-19 and depressive symptoms was merely driven by somatic symptoms of depression and did not follow a gradient consistent with the hypothesis of a direct impact of SARS-CoV-2 infection on the risk of depression.

Most psychiatric disorders are associated with several risk factors, but a few underlying psychopathological dimensions account for the common co-occurrence of disorders. If these underlying psychopathological dimensions mediate associations of the risk factors with psychiatric disorders, it would support a trans-diagnostic orientation to etiological research and treatment development.

An analysis was performed of the 2012–2013 National Epidemiologic Survey on Alcohol and Related Conditions III (NESARC-III), a US nationally representative sample of non-institutionalized civilian adults, focusing on respondents who were aged ⩾21 (n = 34 712). Structural equation modeling was used to identify the psychopathological dimensions underlying psychiatric disorders; to examine associations between risk factors, psychopathological dimensions and individual disorders; and to test whether associations of risk factors occurring earlier in life were mediated by risk factors occurring later in life.

A bifactor model of 13 axis I disorders provided a good fit (CFI = 0.987, TLI = 0.982, and RMSEA = 0.011) including an overall psychopathology factor as measured by all 13 disorders and 2 specific factors, one for externalizing disorders and one for fear-related disorders. A substantial proportion of the total effects of the risk factors occurring early in life were indirectly mediated through factors occurring later in life. All risk factors showed a significant total effect on the general psychopathology, externalizing and fear-related factors. Only 23 of 325 direct associations of risk factors with psychiatric disorders achieved statistical significance.

Most risk factors for psychiatric disorders are mediated through broad psychopathological dimensions. The central role of these dimensions supports trans-diagnostic etiological and intervention research.

Neuroimaging studies of vulnerability to Alcohol Use Disorder (AUD) have identified structural and functional variations which might reflect inheritable features in alcohol-naïve relatives of AUD individuals (FH+) compared to controls having no such family history (FH-). However, prior research did not simultaneously account for childhood maltreatment, any clinically significant disorder and maternal AUD. Therefore, we mainly aimed to investigate the brain structure and reward-related neural activations (fMRI), using whole-brain analysis in FH+ young adults with no prevalent confounders.

46 FH+ and 45 FH- male and female participants had no severe childhood maltreatment exposure, neither any psychiatric disorder or AUD, nor a prenatal exposure to maternal AUD. We used a 3 T MRI coupled with a whole brain voxel-based method to compare between groups the grey matter volumes and activations in response to big versus small wins during a Monetary Incentive Delay task. The Childhood Trauma Questionnaire score was used as confounding variable in the analyses to account for the remaining variance between groups.

Compared to FH- controls, FH+ participants had smaller grey matter volumes in the frontal and cingulate regions as well as in the bilateral nucleus accumbens and right insula. The FH+ participants’ fMRI datasets denoted a blunted activation in the middle cingulum with respect to FH- controls’ during the processing of reward magnitude, and a greater activation in the anterior cingulum in response to anticipation of a small win.

Family history of alcohol use disorder is linked to structural and functional variations including brain regions involved in reward processes.

Data on psychotropic medications of older patients with schizophrenia spectrum disorder are scarce. Specifically, information about the use of benzodiazepines among older patients with schizophrenia spectrum disorder is very limited. Because benzodiazepine use in older patients has been associated with many disabling side effects, its use in actual practice must be described and questioned. This study aimed at exploring the prevalence of benzodiazepine use and the clinical factors associated with such use among older patients with schizophrenia spectrum disorder.

Data from the Cohort of individuals with Schizophrenia Aged 55 years or more (CSA) were used to examine the prevalence of benzodiazepine use among older patients with schizophrenia spectrum disorder. Demographic and clinical characteristics associated with benzodiazepine prescription were also explored.

The prevalence of benzodiazepine use was 29.8% of older patients with schizophrenia spectrum disorder. These patients were significantly more likely to have medical comorbidities, cognitive and social functioning impairments, to report a lifetime history of suicide attempt, to be institutionalized, and to have been hospitalized in a psychiatric service in the past year compared to those without a benzodiazepine prescription (all p<0.05). There were no between-group differences in schizophrenia severity and psychiatric comorbidity.

Although it can be hypothesized that benzodiazepine prescription is part of a short-term therapeutic strategy toward patients with more severe trouble or comorbid disorders, our results suggest a strong link between benzodiazepine prescription and a particularly vulnerable subpopulation of older patients with schizophrenia spectrum disorder.