Child maltreatment is associated with increased risk for psychiatric disorders, and a range of health problems later in life. The aim of this paper is to review emerging data on the role of epigenetic mechanisms in the etiology of stress-related psychiatric disorders with a focus on future avenues of investigation. Epigenetic processes are described, key findings in the field presented, clinical implications of the research discussed, methodological issues, and future avenues of research considered. Research suggests that adverse early experiences can lead to changes in gene expression through epigenetic mechanisms that can alter stress reactivity, brain function, and behavior. While these changes are frequently long lasting, they can be reversed through pharmacological and environmental manipulations. The complexity of the epigenome is not fully understood. Future studies should investigate epigenetic marks other than methylcytosine, and assess the efficacy of interventions to reverse epigenetic processes associated with early-life adversity.
Background:There is robust evidence that schizophrenia is characterized by immune-inflammatory abnormalities, including variations on cytokine levels. The results of previous studies, however, are heterogeneous due to several confounding factors, such as the effects of antipsychotic drugs. Therefore, research on drug-naïve first-episode psychosis (FEP) patients is essential to elucidate the role of immune processes in that disorder.Methods:The aim of this study is to compare cytokine levels (IL-2, IL-10, IL-4, IL-6, IFN-γ, TNF-α, and IL-17) in drug-naïve FEP patients both before and after treatment with risperidone for 10 weeks, and to investigate possible associations between cytokine levels and clinical responses to treatment and presence of depressive symptoms. It this study, we included 55 drug-naïve FEP patients who had repeated measurements of cytokine levels and 57 healthy controls.Results:We found that FEP patients had significantly higher IL-6, IL-10 and TNF-α levels than healthy controls. After risperidone treatment, these three cytokines and additionally IL-4 decreased significantly. No significant difference was found between the post-treatment cytokine levels in FEP patients and in healthy controls, suggesting that these alterations in cytokine profiles are a state marker of FEP. No significant association was found between risperidone-induced changes in cytokines and the clinical response to treatment or the presence of depression. There was a significant inverse association between the risperidone-induced changes in IL-10 and the negative symptoms.Conclusions:In conclusion, our results show a specific cytokine profile in FEP patients (monocytic and regulatory T-cell activation) and suggest immunoregulatory effects of risperidone treatment, characterized by suppressant effects on monocytic, Th2, and T-regulatory functions.
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