, 11 "Centro per lo studio dei meccanismi molecolari alla base delle patologie neuro-psico-geriatriche",

C.M.); zoccali@unime.it (R.A.Z.); mmuscatello@unime.it (M.R.A.M.)Abstract: The transition to parenthood is considered to be a major life transition that can increase the vulnerability to parental depressive disorders, including paternal perinatal depression (PPND).Although it is known that many fathers experience anxiety and depression during the perinatal period, PPND is a recent diagnostic entity and there are not enough published studies on it. Accordingly, its prevalence and epidemiology are still not well defined, although the majority of studies agree that PPND is less frequent than maternal perinatal depression and postpartum depression. Nevertheless, PPND is different from maternal perinatal mental health disorders, usually, fathers have less severe symptoms, and mood alterations are often in comorbidity with other affective disorders. Despite the absence of DSM-5 diagnostic criteria and the fluctuation of prevalence rates, clinical symptoms have been defined. The main symptoms are mood alterations and anxiety, followed by behavioral disturbances and concerns about the progress of pregnancy and the child's health. Moreover, PPND negatively impacts on family functioning, on couples' relationships, and on family members' well-being. The aim of this paper is to present an overview of the current understandings on PPND and the potential screening, prevention, and treatment options.

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Background Obsessive–compulsive disorder (OCD) is a prevalent and severe clinical condition. Robust evidence suggests a gene-environment interplay in its etiopathogenesis, yet the underlying molecular clues remain only partially understood. In order to further deepen our understanding of OCD, it is essential to ascertain how genes interact with environmental risk factors, a cross-talk that is thought to be mediated by epigenetic mechanisms. The human microbiota may be a key player, because bacterial metabolites can act as epigenetic modulators. We analyzed, in the blood and saliva of OCD subjects and healthy controls, the transcriptional regulation of the oxytocin receptor gene and, in saliva, also the different levels of major phyla. We also investigated the same molecular mechanisms in specific brain regions of socially isolated rats showing stereotyped behaviors reminiscent of OCD as well as short chain fatty acid levels in the feces of rats. Results Higher levels of oxytocin receptor gene DNA methylation, inversely correlated with gene expression, were observed in the blood as well as saliva of OCD subjects when compared to controls. Moreover, Actinobacteria also resulted higher in OCD and directly correlated with oxytocin receptor gene epigenetic alterations. The same pattern of changes was present in the prefrontal cortex of socially-isolated rats, where also altered levels of fecal butyrate were observed at the beginning of the isolation procedure. Conclusions This is the first demonstration of an interplay between microbiota modulation and epigenetic regulation of gene expression in OCD, opening new avenues for the understanding of disease trajectories and for the development of new therapeutic strategies.