Schizophrenia, depression and posttraumatic stress disorder (PTSD) are severe mental disorders and complicated diagnostic entities, due to their phenotypic, biological and genetic heterogeneity, unknown etiology, and poorly understood alterations in biological pathways and biological mechanisms. Disturbed homeostasis between overproduction of oxidant species, overcoming redox regulation and a lack of cellular antioxidant defenses, resulting in free radical-mediated pathology and subsequent neurotoxicity contributes to development of depression, schizophrenia and PTSD, their heterogeneous clinical presentation and resistance to treatment. Metabolomics is a discipline that combines different strategies with the aim to extract, detect, identify and quantify all metabolites that are present in a biological sample and might provide mechanistic insights into the etiology of various psychiatric disorders. Therefore, oxidative stress research combined with metabolomics might offer a novel approach in dissecting psychiatric disorders, since these data-driven but not necessarily hypothesis-driven methods might identify new targets, molecules and pathways responsible for development of schizophrenia, depression or PTSD. Findings from the oxidative research in psychiatry together with metabolomics data might facilitate development of specific and validated prognostic, therapeutic and clinical biomarkers. These methods might reveal bio-signatures of individual patients, leading to individualized treatment approach. In reviewing findings related to oxidative stress and metabolomics in selected psychiatric disorders, we have highlighted how these novel approaches might make a unique contribution to deeper understanding of psychopathological alterations underlying schizophrenia, depression and PTSD.

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Posttraumatic stress disorder (PTSD) is a stressor-related disorder that develops in a subset of individuals exposed to a traumatic experience. Factors associated with vulnerability to PTSD are still not fully understood. PTSD is frequently comorbid with various psychiatric and somatic disorders, moderate response to treatment and remission rates. The term "theranostics" combines diagnosis, prognosis, and therapy and offers targeted therapy based on specific analyses. Theranostics, combined with novel techniques and approaches called "omics", which integrate genomics, transcriptomic, proteomics and metabolomics, might improve knowledge about biological underpinning of PTSD, and offer novel therapeutic strategies. The focus of this review is on metabolomic and glycomic data in PTSD. Metabolomics evaluates changes in the metabolome of an organism by exploring the set of small molecules (metabolites), while glycomics studies the glycome, a complete repertoire of glycan structures with their functional roles in biological systems. Both metabolome and glycome reflect the physiological and pathological conditions in individuals. Only a few studies evaluated metabolic and glycomic changes in patients with PTSD. The metabolomics studies in PTSD patients uncovered different metabolites that might be associated with psychopathological alterations in PTSD. The glycomics study in PTSD patients determined nine N-glycan structures and found accelerated and premature aging in traumatized subjects and subjects with PTSD based on a GlycoAge index. Therefore, further larger studies and replications are needed. Better understanding of the biological basis of PTSD, including metabolomic and glycomic data, and their integration with other "omics" approaches, might identify new molecular targets and might provide improved therapeutic approaches.

Better understanding of the role of COMT in cognitive processes in AD, as well as integration of neurobiological, genetic, genomic and epigenetic data, might help in developing new potential therapies of cognitive impairments and psychotic symptoms, characteristic features of AD.

Background: Sporadic Alzheimer’s Disease (AD) is assumed to be associated with different biological/genetic vulnerability, as well as with neuroinflammation, mediated by cytokines. The present study evaluated the role of cytokines in AD. Objective: Aim was to determine the possible association of TNF-α (rs1800629), IL1-α (rs1800587) and IL-10 (rs1800896) polymorphisms with AD, and to assess serum TNF-α, IL-1α and IL-10 concentrations in patients with AD and in subjects with mild cognitive impairment (MCI). Method: The study included 645 Caucasian participants: 395 subjects with AD and 250 subjects with MCI. Genotyping was performed using real time PCR in all 645 subjects, while serum concentrations of TNF-α, IL-1α and IL-10 and were determined using ELISA in 174 subjects. Results: The frequency of the TNF-ɑ rs1800629, IL1-ɑ rs1800587 or IL-10 rs1800896 genotypes did not differ significantly between patients with AD and MCI. Serum concentration of IL-1α and IL-10 were significantly decreased, while the concentration of TNF-α was significantly higher in patients with AD than in MCI subjects. TNF-α, IL1-α or IL-10 concentrations were similar in subjects with AD or MCI subdivided into carriers of the corresponding TNF-ɑ rs1800629, IL1-ɑ rs1800587 or IL-10 rs1800896 genotypes. Conclusions: Similar distribution of the IL1-ɑ rs1800587, TNF-ɑ rs1800629 or IL-10 rs1800896 genotypes in subjects with AD and MCI failed to confirm that these specific risk genotypes are associated with vulnerability to develop AD. Alteration in IL-1α, IL-10 and TNF-α concentrations in patients with AD partially confirmed the association with neuroinflammatory response in AD.