A genetic contribution to the pathogenesis of panic disorder has been demonstrated by clinical genetic studies. Molecular genetic studies have focused on candidate genes suggested by the molecular mechanisms implied in the action of drugs utilized for therapy or in challenge tests. One class of drugs effective in the treatment of panic disorder is represented by monoamine oxidase A inhibitors. Therefore, the monoamine oxidase A gene on chromosome X is a prime candidate gene. In the present study we investigated a novel repeat polymorphism in the promoter of the monoamine oxidase A gene for association with panic disorder in two independent samples (German sample, n = 80; Italian sample, n = 129). Two alleles (3 and 4 repeats) were most common and constituted >97% of the observed alleles. Functional characterization in a luciferase assay demonstrated that the longer alleles (3a, 4 and 5) were more active than allele 3. Among females of both the German and the Italian samples of panic disorder patients (combined, n = 209) the longer alleles (3a, 4 and 5) were significantly more frequent than among females of the corresponding control samples (combined, n = 190, chi2 = 10.27, df = 1, P = 0.001). Together with the observation that inhibition of monoamine oxidase A is clinically effective in the treatment of panic disorder these findings suggest that increased monoamine oxidase A activity is a risk factor for panic disorder in female patients.

Comorbidity with anxiety or depression is common in patients with Inflammatory Bowel Disease (IBD) as Crohn Disease (CD) and Ulcerative Colitis (UC). Data suggest that the cognitive construct of alexithymia has high prevalence in people suffering from anxiety and mood disorders and even in people with IBD. Most studies have investigated mainly anxiety and depression, considering IBD population as a homogeneous group of patients. Little evidence shows the impact of alexithymia on the course of IBD. We evaluated a broad spectrum of psychopathological symptoms and alexithymia levels in a group of outpatients affected by IBD in clinical remission, comparing CD and UC and investigating the relationship with clinical and socio-demographic variables. One hundred and seventy IBD outpatients were screened by using the Hospital Anxiety Depression Scale (HADS), the Self-report Symptom Inventory-90-Revised (SCL-90-R) and the Toronto Alexithymia Scale (TAS-20). A high prevalence of anxious and depressive symptoms (42.35 and 25.8% respectively) together with alexithymia (31.76%) was confirmed. CD patients experienced high levels of depression (HADS Depression 35.2% p = 0.034; SCL-90-R mean 1.39 p < 0.001), somatisation (SCL-90-R mean 1.04 p < 0.001), obsessive-compulsive symptoms (SCL-90-R mean 1.2 p < 0.001), and global severity (SCL-90-R mean 1.15 p < 0.001). There is no statistical difference in the prevalence of alexithymia in both subpopulations. The levels of alexithymia are correlated to the levels of anxiety (HADS Anxiety rs = 0.516 p < 0.001), depression (HADS Depression rs = 0.556 p < 0.001; SCL-90-R rs = 0.274 p = 0.001), somatisation (SCL-90-R rs = 0.229 p = 0.005), obsessive-compulsive symptoms (SCL-90-R rs = 0.362 p < 0.001), and global severity (SCL-90-R rs = 0.265 p = 0.001). Furthermore, alexithymia is associated with a delay of diagnosis of IBD, poly-therapies and greater IBD extension. Older age, female gender, greater IBD extension, surgery, and delay of diagnosis seem to be related to a high prevalence of psychopathological symptoms such as anxiety, depression, somatisation, and obsessive-compulsive symptoms. Psychopathological symptoms and high levels of alexithymia are frequent in IBD patients and seem to be related to a high risk of poor clinical outcome. CD patients could be considered at higher risk of mental comorbidity. A more comprehensive psychiatric assessment, including alexithymia, and an integrated treatment of underlying conditions, must be taken into account in order to improve the global prognosis of the disease.

Objective: Some studies have linked the use of selective serotonin reuptake inhibitors and selective serotonin and noradrenaline reuptake inhibitors (SSRIs/ SNRIs) to the risk of perinatal complications. This study explored the relationship between pharmacokinetics and pharmacogenetics, SSRIs/SNRIs tolerability and effectiveness and maternal and newborn outcomes.Methods: Fifty-five pregnant women with Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) diagnoses of affective disorders, treated with SSRIs/SNRIs, were recruited and, during the third trimester, their blood samples were collected for pharmacokinetic and pharmacogenetic analyses. Plasma levels and metabolic phenotypes were then related to different obstetrical and maternal outcomes. Results:The pharmacokinetic data were more stable for Sertraline, Citalopram, and Escitalopram compared to other molecules (p = 0.009). The occurrence of postnatal adaptation syndrome onset was associated with higher plasma levels for Sertraline (median at delivery: 16.7 vs. 10.5 ng/ml), but not for fluoxetine and venlafaxine.Finally, the subgroup within range plasma concentrations had less blood loss than the below range subgroup (p = 0.030).Conclusions: Plasma levels of Sertraline, Citalopram and Escitalopram were more frequently in range in late pregnancy when compared to other drugs. Drug plasma concentrations do not strictly correlate with worse perinatal outcomes, but with possible differences between the different drugs.

Objective: Despite growing evidence in the field of cognitive function in mood disorders, the neurocognitive profiles of patients with unipolar and bipolar depression still need further characterization. In this study, we applied network analysis, hypothesizing this approach could highlight differences between Major Depressive Disorder (MDD) and Bipolar Disorder (BD) from a cognitive perspective. Methods: The cognitive performance of 109 patients (72 unipolar and 37 bipolar depressed outpatients) was assessed through the Montreal Cognitive Assessment (MoCA) and a series of clinical variables was collected. Differences in cognitive performance between MDD and BD patients were tested using non parametric tests. Moreover, a network graph representing MoCA domains as nodes and Spearman's rho correlation coefficients between the domains as edges was constructed for each group. Results: The presence of mild cognitive impairment was observed both in MDD and BD patients during depression. No statistical significant difference was found between the two groups in terms of overall cognitive performance and across single domains. Nonetheless, network analytic metrics demonstrated different roles of memory and executive dysfunction in MDD vs BD patients: in particular, MDD network was more densely interconnected than BD network and memory was the node with the highest betweenness and closeness centrality in MDD, while executive function was more central in BD. Conclusions:From a network analytic perspective, memory impairment displays a central role in the cognitive impairment of patients with unipolar depression, whereas executive dysfunction appears to be more central in bipolar depression. Further research is warranted to confirm our results.