期刊
SCHIZOPHRENIA BULLETIN
卷 42, 期 2, 页码 386-395出版社
OXFORD UNIV PRESS
DOI: 10.1093/schbul/sbv134
关键词
Toxoplasma gondii; animal model; biomarker
类别
资金
- Stanley Medical Research Institute
- European Union [286334]
- Virgo consortium
- Dutch Government [FES0908]
- Netherlands Genomics Initiative [050-060-452]
- Dutch Fund for Economic Structure Reinforcement, the NeuroBasic PharmaPhenomics project [0908]
Chronic neurologic infection with Toxoplasma gondii is relatively common in humans and is one of the strongest known risk factors for schizophrenia. Nevertheless, the exact neuropathological mechanisms linking T gondii infection and schizophrenia remain unclear. Here we utilize a mouse model of chronic T gondii infection to identify protein biomarkers that are altered in serum and brain samples at 2 time points during chronic infection. Furthermore, we compare the identified biomarkers to those differing between postmortem brain samples from 35 schizophrenia patients and 33 healthy controls. Our findings suggest that T gondii infection causes substantial and widespread immune activation indicative of neural damage and reactive tissue repair in the animal model that partly overlaps with changes observed in the brains of schizophrenia patients. The overlapping changes include increases in C-reactive protein (CRP), interleukin-1 beta (IL-1 beta), interferon gamma (IFN gamma), plasminogen activator inhibitor 1 (PAI-1), tissue inhibitor of metalloproteinases 1 (TIMP-1), and vascular cell adhesion molecule 1 (VCAM-1). Potential roles of these factors in the pathogenesis of schizophrenia and toxoplasmosis are discussed. Identifying a defined set of markers shared within the pathophysiological landscape of these diseases could be a key step towards understanding their specific contributions to pathogenesis.
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