Data is progressively and robustly accumulating regarding the biological basis of autism. Autism spectrum disorders (ASD) are currently considered a group of neurodevelopmental disorders with onset very early in life and a complex, heterogeneous, multifactorial aetiology. A comprehensive search of the last five years of the Medline database was conducted in order to summarize recent evidence on the neurobiological bases of autism. The main findings on genetic influence, neuropathology, neurostructure and brain networks are summarized. In addition, findings from peripheral samples of subjects with autism and animal models, which show immune, oxidative, mitochondrial dysregulations, are reported. Then, other biomarkers from very different systems associated with autism are reported. Finally, an attempt is made to try and integrate the available evidence, which points to a oligogenetic, multifactorial aetiology that converges in an aberrant micro-organization of the cortex, with abnormal functioning of the synapses and abnormalities in very general physiological pathways (such as inflammatory, immune and redox systems).

Elevated number of parental Communication Deviance (CD) has been connected with psychiatric and thought disorders in their offspring. However, no earlier systematic efforts have been made to review this issue. The aim of this study was to survey the existing literature systematically and perform a meta-analysis of this association. A literature search for published and unpublished observational studies on the association of parental Communication Deviance with psychopathology in the offspring was conducted. Multiple electronic databases were searched (from 1960 to 2012) and the reference lists of the resulting publications were scanned. The findings were pooled using random effect meta-analysis. A total of 19 relevant papers were found and accessed. The results showed that a high level of parental CD is associated with schizophrenia spectrum disorders in the offspring. A large overall effect size (0.79) was found in the meta-analysis. No meta-analysis could be performed on the association of parental CD with an offspring's thought disorders, but the results suggest that such an association may exist. Parental Communication Deviance is associated with schizophrenia spectrum disorders in the offspring. High parental CD could be treated as an indicator of a risk of developing a schizophrenia spectrum disorder, at least among high-risk groups.

This study investigated the relationship between severe childhood abuse and cognitive functions in first-episode psychosis patients and geographically-matched controls. Reports of any abuse were associated with lower scores in the executive function domain in the control group. However, in contrast with our hypothesis, no relationships were found amongst cases.

Many family characteristics were reported to increase the risk of bipolar disorder (BPD). The development of BPD may be mediated through different pathways, involving diverse risk factor profiles. We evaluated the associations of family characteristics to build influential causal-pie models to estimate their contributions on the risk of developing BPD at the population level. We recruited 329 clinically diagnosed BPD patients and 202 healthy controls to collect information in parental psychopathology, parent-child relationship, and conflict within family. Other than logistic regression models, we applied causal-pie models to identify pathways involved with different family factors for BPD. The risk of BPD was significantly increased with parental depression, neurosis, anxiety, paternal substance use problems, and poor relationship with parents. Having a depressed mother further predicted early onset of BPD. Additionally, a greater risk for BPD was observed with higher numbers of paternal/maternal psychopathologies. Three significant risk profiles were identified for BPD, including paternal substance use problems (73.0%), maternal depression (17.6%), and through poor relationship with parents and conflict within the family (6.3%). Our findings demonstrate that different aspects of family characteristics elicit negative impacts on bipolar illness, which can be utilized to target specific factors to design and employ efficient intervention programs.

The present study aimed to determine whether any gender-related difference exists concerning oxidative stress parameters in a population of 231 subjects, and if these changes might be related to gender-associated differences in major depressive disorder (MDD) or bipolar disorder (BD) vulnerability. This is a case-control nested in a population-based study. The initial psychopathology screen was performed with the Mini-International Neuropsychiatric Interview and the diagnostic was further confirmed with the Structured Clinical Interview for DSM-IV. Blood samples were obtained after the interview and the oxidative stress parameters such as uric acid, advanced oxidation protein product (PCC) and lipid hydroperoxides (TBARS) were determined. Our results indicated a higher prevalence of MDD and BD in women when compared to men. In addition, significant gender differences were found in the levels of PCC (0.27 ± 0.27 vs. 0.40 ± 0.31 nmol CO/mg protein, men vs. women, respectively; P = 0.02) and uric acid (4.88 ± 1.39 mg/dL vs. 3.53 ± 1.02 mg/dL, men vs. women, respectively; P = 0.0001), but not in TBARS (0.013 ± 0.01 nmol/mg of protein vs. 0.017 ± 0.02 nmol/mg of protein, men vs. women respectively; P = 0.243). After sample stratification by gender, no association was found between oxidative stress parameters and clinical diagnosis of MDD and BD for women (P = 0.516 for PCC; P = 0.620 for TBARS P = 0.727 for uric acid) and men (P = 0.367 for PCC; P = 0.372 for TBARS P = 0.664 for uric acid). In this study, women seem more susceptible to oxidative stress than male. However, these gender-based differences do not seem to provide a biochemical basis for the epidemiologic differences in mood disorders susceptibility between sexes.