The human social brain is complex. Current knowledge fails to define the neurobiological processes underlying social behaviour involving the (patho-) physiological mechanisms that link system-level phenomena to the multiple hierarchies of brain function. Unfortunately, such a high complexity may also be associated with a high susceptibility to several pathogenic interventions. Consistently, social deficits sometimes represent the first signs of a number of neuropsychiatric disorders including schizophrenia (SCZ), Alzheimer's disease (AD) and major depressive disorder (MDD) which leads to a progressive social dysfunction. In the present review we summarize present knowledge linking neurobiological substrates sustaining social functioning, social dysfunction and social withdrawal in major psychiatric disorders. Interestingly, AD, SCZ, and MDD affect the social brain in similar ways. Thus, social dysfunction and its most evident clinical expression (i.e., social withdrawal) may represent an innovative transdiagnostic domain, with the potential of being an independent entity in terms of biological roots, with the perspective of targeted interventions.

Background: Dementia shows sex difference in its epidemiology. Childbirth, a distinctive experience of women, is associated with the risk for various diseases. However, its association with the risk of dementia in women has rarely been studied. Methods: We harmonized and pooled baseline data from 11 population-based cohorts from 11 countries over 3 continents, including 14,792 women aged 60 years or older. We investigated the association between parity and the risk of dementia using logistic regression models that adjusted for age, educational level, hypertension, diabetes mellitus, and cohort, with additional analyses by region and dementia subtype. Results: Across all cohorts, grand multiparous (5 or more childbirths) women had a 47% greater risk of dementia than primiparous (1 childbirth) women (odds ratio [OR] = 1.47, 95% confidence interval [CI] = 1.10–1.94), while nulliparous (no childbirth) women and women with 2 to 4 childbirths showed a comparable dementia risk to primiparous women. However, there were differences associated with region and dementia subtype. Compared to women with 1 to 4 childbirths, grand multiparous women showed a higher risk of dementia in Europe (OR = 2.99, 95% CI = 1.38–6.47) and Latin America (OR = 1.49, 95% CI = 1.04–2.12), while nulliparous women showed a higher dementia risk in Asia (OR = 2.15, 95% CI = 1.33–3.47). Grand multiparity was associated with 6.9-fold higher risk of vascular dementia in Europe (OR = 6.86, 95% CI = 1.81–26.08), whereas nulliparity was associated with a higher risk of Alzheimer disease (OR = 1.91, 95% CI 1.07–3.39) and non-Alzheimer non-vascular dementia (OR = 3.47, 95% CI = 1.44–8.35) in Asia. Conclusion: Parity is associated with women’s risk of dementia, though this is not uniform across regions and dementia subtypes.

The authors evaluated the association of low-to-moderate alcohol consumption with risk of cognitive decline in a census-based cohort study of men and women aged ≥55 years conducted in Zaragoza, Spain (1994–1999). Participants free of dementia at baseline (N = 3,888) were examined after 2.5 and 4.5 years of follow-up. Information on alcohol intake was collected with the EURODEM Risk Factors Questionnaire and the History and Aetiology Schedule. The study endpoint was severe cognitive decline, defined as loss of ≥1 point/year on the Mini-Mental State Examination or a diagnosis of incident dementia (Diagnostic and Statistical Manual of Mental Disorders: DSM-IV, Text Revision criteria). Compared with those for abstainers, the multivariate-adjusted odds ratios for severe cognitive decline for male drinkers of <12 g alcohol/day, drinkers of 12–24 g alcohol/day, and former drinkers were 0.61 (95% confidence interval (CI): 0.31, 1.20), 1.19 (95% CI: 0.61, 2.32), and 1.03 (95% CI: 0.59, 1.82), respectively. The corresponding odds ratios for women were 0.88 (95% CI: 0.45, 1.72), 2.38 (95% CI: 0.98, 5.77), and 1.03 (95% CI: 0.48, 2.23). This study did not support the hypothesis that low-to-moderate alcohol consumption prevents cognitive decline. The inverse association between low-to-moderate alcohol intake and cognitive decline observed in other studies may have been due to inclusion of former drinkers in the abstainers reference category.