ArticleThe Journal of international medical research2017
First description of enhanced expression of glia maturation factor-beta in experimental toxoplasmic encephalitis.
Article in The Journal of international medical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- Platelet Rich Plasma as a Potential Therapy for Chronic Toxoplasmosis in Immunocompetent and Immunocompromised Murine Model.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Contribution of the dopaminergic system in toxoplasmic encephalitis neuroimmunopathogenesis.Histology and histopathology · 2025Article
- First Description of the Role of the Relationship Between Serum Amyloid P Components and Nuclear Factors/Pro-Cytokines During Critical Periods of Toxoplasmic Encephalitis.Brain sciences · 2024Article
- Ginger Is a Potential Therapeutic for Chronic Toxoplasmosis.Pathogens (Basel, Switzerland) · 2022Article
- Rosuvastatin reduced brain parasite burden in a chronic toxoplasmosisParasitology · 2020Article
- Proteomics in Schizophrenia: A Gateway to Discover Potential Biomarkers of Psychoneuroimmune Pathways.Frontiers in psychiatry · 2019Article
- Co Expression ofIranian journal of parasitologyArticle
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective We previously showed that Toxoplasma gondii infection induces severe neuropathology in the form of oxidative stress, high nitric oxide production, glial activation, and apoptosis. This study examined the association between glia maturation factor-beta (GMF-β) expression, activated astrocytes/microglia, and neuropathology in toxoplasmic encephalitis (TE). Methods Mouse brain GMF expression was examined by immunohistochemistry on days 10 and 30 post- T. gondii infection. Results Neuropathology of infected mice was associated with increased GMF expression in reactive glial cells and neurons compared with healthy controls. Specific up-regulation of GMF-β expression in glial cells was associated with increased gliosis in TE. Conclusions GMF up-regulation in glial cells causes neuronal destruction, suggesting a TE pathological pathway involving GMF-mediated brain cell cytotoxicity. GMF-β may therefore be a good biomarker for disease risk assessment and to estimate host neuropathy after exposure to T. gondii, as well as providing a new therapeutic target. This is the first study to demonstrate the expression of GMF-β in reactive glial cells and its association with neuropathology in TE.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.