Genetic and environmental risk factors in neurodevelopmental disorders.

Abstract

participants underwent three stressing conditions under which they performed parallel versions of cognitive bias tasks. Under stress, particularly noise, patients in comparison with controls showed an increased jumping to conclusion bias and made more monocausal attributions, increasing under social stress. Since stress seems to negatively affect cognition in psychosis, increasing patient’s awareness in this regard might be beneficial for improving positive symptoms. The incidence of psychotic symptoms in the general population is more common than validly diagnosed psychoses and might be associated with the same risk factors. Traumatic stress experience and symptoms of post-traumatic stress disorder (PTSD) have recently been suggested to be related to schizophrenia risk. Ayub et al. [3] conducted a cross-sectional survey in 1291 persons 1.5 years after an earthquake. The association between symptoms of anxiety, depression, PTSD, and psychotic symptoms via logistic regression analysis showed psychotic symptoms to be directly correlated with symptoms of PTSD as well as concurrent symptoms of anxiety and depression. Lower educational level was strongly associated with all regression models. Opposite to a positive association of previous traumatic exposure or past psychiatric history, living in a joint family was negatively associated with hallucinations. In accordance with prior correspondent publications, paranoia was associated with female gender, any other psychiatric symptom with environmental stress factors or history of past psychiatric illness. Modelling stressors in animal models can be helpful in dissecting gene–environment relationships, but underlie practical limitations which afford protocol standardization as well as appropriate statistical normalization to compare different experiments. To this respect, Badowska et al. [4] merged data of individual measures in two independent wild-type mice studies on psychosocial stress into broader According to the immune hypothesis of schizophrenia, an immune system deregulation possibly influences the risk of schizophrenia. For this reason, Frydecka et al. [1] investigated the influence of serum interleukin-6 (IL-6) level together with the polymorphism in its gene (IL-6–174G/C) plus high-sensitivity C-reactive protein (hsCRP) levels on clinical manifestation and cognition in 151 schizophrenia patients and 194 healthy controls. Compared to controls, patients showed significantly higher serum IL-6 and hsCRP levels and both also were significantly associated with insidious psychosis onset, duration of illness, and chronic plus deteriorating course of schizophrenia. The association between IL-6 and hsCRP and worse cognitive performance also remained positive after complex adjustment, whereas the IL-6–174G/C polymorphism had no influence on the IL-6 level albeit on the severity of positive symptoms. Hence, elevated IL-6 levels are possibly relevant in cognitive impairment and a potential inflammatory biomarker of deterioration in schizophrenia. Besides the effects of risk genes, an interaction with environmental factors such as psychosocial stress plays a role in the pathophysiology of schizophrenia. Since stress seems to be complexly linked to psychotic breakdown, Moritz et al. [2] studied the relevance of two cognitive core biases in psychosis in 30 schizophrenia patients with acute delusional symptoms compared to 29 healthy controls. Added by neuropsychological tests,