Schizophrenia is a highly heritable, chronic, severe, disabling neurodevelopmental brain disorder with a heterogeneous genetic and neurobiological background, which is still poorly understood. To allow better diagnostic procedures and therapeutic strategies in schizophrenia patients, use of easy accessible biomarkers is suggested. The most frequently used biomarkers in schizophrenia are those associated with the neuroimmune and neuroendocrine system, metabolism, different neurotransmitter systems and neurotrophic factors. However, there are still no validated and reliable biomarkers in clinical use for schizophrenia. This review will address potential biomarkers in schizophrenia. It will discuss biomarkers in schizophrenia and propose the use of specific blood-based panels that will include a set of markers associated with immune processes, metabolic disorders, and neuroendocrine/neurotrophin/neurotransmitter alterations. The combination of different markers, or complex multi-marker panels, might help in the discrimination of patients with different underlying pathologies and in the better classification of the more homogenous groups. Therefore, the development of the diagnostic, prognostic and theranostic biomarkers is an urgent and an unmet need in psychiatry, with the aim of improving diagnosis, therapy monitoring, prediction of treatment outcome and focus on the personal medicine approach in order to improve the quality of life in patients with schizophrenia and decrease health costs worldwide.

(2013) The lack of association between components of metabolic syndrome and treatment resistance in depression. npivac@irb.hr Psychopharmacology, 230 (1). Conflicts of Interest:Authors declare no conflict of interest. All authors state that they have full control of all primary data and that they agree to allow the journal to review this data. Acknowledgments:This study was supported by the Croatian Ministry of Science, Education and Sport, grants numbers 098-0982522-2455; 098-0982522-2457; 109-1083509-3513; 108-1083509-3511.

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.

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.