Abstract
Schizophrenia is a very complex syndrome involving widespread brain multi-dysconnectivity. Schizophrenia is marked by cognitive, behavioral, and emotional dysregulations. Recent studies suggest that inflammation in the central nervous system (CNS) and immune dysfunction could have a role in the pathogenesis of schizophrenia. This hypothesis is supported by immunogenetic evidence, and a higher incidence rate of autoimmune diseases in patients with schizophrenia. The dysregulation of the WNT/β-catenin pathway is associated with the involvement of neuroinflammation in schizophrenia. Several studies have shown that there is a vicious and positive interplay operating between neuroinflammation and oxidative stress. This interplay is modulated by WNT/β-catenin, which interacts with the NF-kB pathway; inflammatory factors (including IL-6, IL-8, TNF-α); factors of oxidative stress such as glutamate; and dopamine. Neuroinflammation is associated with increased levels of PPARγ. In schizophrenia, the expression of PPAR-γ is increased, whereas the WNT/β-catenin pathway and PPARα are downregulated. This suggests that a metabolic-inflammatory imbalance occurs in this disorder. Thus, this research’s triptych could be a novel therapeutic approach to counteract both neuroinflammation and oxidative stress in schizophrenia.
Highlights
Schizophrenia is a neurodevelopmental and mental illness affecting nearly 1% of the world’s population, and the age of onset age is between 23 and 34 years in women and close to 30 years in men [1]
Redox dysfunction leading to oxidative stress in schizophrenia [102,108] is characterized by the low expression of polyunsaturated fatty acids (PUFAs) in red blood cells during the acute phase of schizophrenia [108]
Astrocytes remove more than 90% of excess glutamate by EAATs and play a major role in the glutamate/glutamine cycle
Summary
Schizophrenia is a neurodevelopmental and mental illness affecting nearly 1% of the world’s population, and the age of onset age is between 23 and 34 years in women and close to 30 years in men [1]. Schizophrenia is characterized by generalized brain multi-dysconnectivity and marked by abnormal brain development, deregulated neuronal migration, impaired spatial neural arrangement, and the absence of gliosis [2]. This mental disorder is composed of cognitive, behavioral, and emotional disorders, and to be diagnosed with schizophrenia, patients should have two (or more) of the following negative symptoms for a minimum of six months—disorganized speech, grossly disorganized or catatonic behavior—and at least one positive symptom [3]. This review focuses on describing the main role of neuroinflammation in schizophrenia and its relationship with the WNT/β-catenin pathway, which leads to the development of oxidative stress, and highlighting possible therapeutic targets
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