Abstract
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.
Highlights
There are numerous environmental and biological factors that interact with genetic factors and contribute to vulnerability or resilience with respect to the development of mental disorders [1]
These results suggest that careful consideration of present medication use, type and doses is needed in the studies of the HPA axis biomarkers in schizophrenia
There are findings showing the augmentation strategies using DHEA(S) in the treatment of schizophrenia: in studies performed on a small number of patients, addition of DHEA(S) as the augmentation strategy improved somatic health, decreased insulin resistance and inflammatory markers and had positive effects on the quality of life or physical disability [84]. These results confirm that some indicators of metabolic syndrome or insulin resistance, or the hypothalamic–pituitary–adrenal–gonadal axis are present in patients with schizophrenia, and that these neuroendocrine and/or metabolic biomarkers might be used to discriminate between patients with or without the risk for metabolic disorder, improve the understanding of the pathophysiological processes associated with schizophrenia, advance the development of treatments focused on these endocrine and metabolic disorders and help in personalized medicine strategies [14,67]
Summary
There are numerous environmental and biological factors that interact with genetic factors and contribute to vulnerability or resilience with respect to the development of mental disorders [1]. Most psychiatric disorders, including schizophrenia, develop in vulnerable subjects who failed to cope with stress and do not achieve positive outcomes when faced with adversities and stressors [2]. Resilience is modulated by diverse systems (neurotransmitters, neurotrophic factors, hypothalamic–pituitary–adrenal (HPA) axis, immune system, autonomic nervous system, oxidative stress and metabolic markers), working together to recover from various stressors and stressful experiences and to achieve a positive adaptation after exposure to stressors that are presenting as threats to homeostasis [3,4]. One of the major systems involved in the regulation of the stress is the HPA axis, which shows enhanced activity (i.e., increased release of corticotrophin releasing factor (CRH), adrenocorticotrophic hormone (ACTH) and cortisol) as a response to stress [5,6]. The HPA axis is self-regulated, with a negative feedback mechanism which inhibits HPA axis activity; and after the system responses to stress or challenge, the HPA axis returns to its “normal” activity, i.e., homeostasis [5,6]
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