Association of neurobiological and immune serum biomarkers with Toxoplasma gondii infection in patients with schizophrenia

Some studies suggest that Toxoplasma gondii infection may increase the risk of developing schizophrenia. Determining changes in blood biomarker concentrations may provide new insights into the underlying mechanisms associated with Toxoplasma gondii infection in schizophrenia. The aim of the study was to evaluate the concentrations of several serum neurobiological and immune parameters and to identify changes in their concentrations that could potentially be indicators of psychopathologic changes in infection. The concentration of biomarkers was determined in serum from patients with schizophrenia (uninfected n = 50, infected n = 30) and from mentally healthy volunteers (uninfected n = 51, infected n = 29) using multiplex analysis. A number of psychometric scales have been applied to assess the cognitive functioning. No significant associations were between schizophrenia and Toxoplasma gondii infection (p = 0.54; OR = 1.18; 95% CI = 0.69–2.01). However, infected patients with schizophrenia had more severe cognitive impairment compared to uninfected schizophrenia patients (PDQ-20). The group of biomarkers has been identified whose concentration changes were observed only between Toxoplasma gondii–infected healthy individuals and individuals with schizophrenia (neurobiological indicators KLK6, UCHL1, Amyloid beta 1–42 and neurogranin; anti-inflammatory cytokine IL-10; chemokines IL-8 and MIP-1 beta), but not between uninfected groups. The hypothesis was proposed that it is possible to use these indices as indicators of the development of schizophrenic psychopathology in Toxoplasma gondii infection. The associations of blood biomarker concentrations with IgA and IgM antibody levels (chemokine RANTES) and with schizophrenia symptoms (hormone-like messenger KLK6; chemokines IP-10 and GRO alpha) were found. Toxoplasma gondii reactivation leads to a decrease in negative symptomatology and reduced FGF-21 levels in patients with schizophrenia, and increased CNTF and NGF beta levels compared to the latent form.