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April 18, 2007
Analysis of Schizophrenia Link to T. gondii Parasite
Read more... Schizophrenia Causes, Risk Factors & Prevention · Schizophrenia Research Journal Articles
E. Fuller Torrey, John J. Bartko, Zhao-Rong Lun, and Robert H. Yolke took on the task of analyzing data from a multitude of research sources from around the world, studying the connection between infection with a one-celled parasitic organism called Toxoplasma gondii and schizophrenia.
People can get the organism by inhaling or ingesting the oocysts (dormant form) which are shed by infected cats into litter boxes, gardens and sandboxes, or through ingesting (eating) the undercooked meat of sheep, goats, or other animals that had become infected with it from exposure to cats. It had been observed that some individuals who develop adult-onset toxoplasmosis (infection with T. gondii) exhibit delusions and hallucinations.
Torrey, et al. say that the data came from studies carried out over 5 decades in 17 countries employing several different methods of antibody measurement. The data show that the prevalence of antibodies to T. gondii in individuals with schizophrenia is significantly higher - over two times as common - than in individuals without schizophrenia.
The data raises many questions, and some very interesting points are made in the paper.
T. gondii tends to reside in brain neurons, especially the ones called, "glia", which are sometimes referred to has the "helper cells" - heavily involved in forming the scaffold for brain structure, guiding the growth of other brain cells. Glia may be centrally involved in schizophrenia. Next, the authors point out that some antipsychotic drugs used to treat schizophrenia have been shown to inhibit the growth of T. gondii in cell culture. Also discussed is the relationship of winter and spring births to the development of schizophrenia and that toxoplasmosis, like many infectious diseases, also occurs more commonly in the winter and spring months.
Still, the authors point out reasons that all this research is still not definitive as to cause and effect, not the least of which is the fact that the majority of individuals with schizophrenia do not have measurable antibodies to T. gondii. E.F. Torrey and colleagues also raise the point that some individuals who are exposed to T. gondii do not develop schizophrenia.
Questions raised for future research includes investigation of timing -- When might exposure to T. gondii be critical in causing the harm that leads to the development of schizophrenia? A discussion of the article in Schizophrenia Forum points out that:
Authors also cite publications that implicate maternal T. gondii infection in the etiology of schizophrenia. This raises the question whether the presence of antibodies in adults reflects prenatal infection, or whether postnatal infection with T. gondii is also a risk factor.They continue with asking,
What are the underlying mechanisms by which exposure to T. gondii leads to schizophrenia vulnerability, and how do these interact with other risk factors, including genetic factors?
E.F. Torrey et al. end the article with a discussion of possible underlying differences that may be present in people accounting for different reactions to the one-celled organism observed. Addressing why should only some individuals who are exposed to the infectious agent develop schizophrenia, they write:
Possible reasons include differences in genetic susceptibility, organism strain differences, route of infection (eg, ingestion of oocysts from infected cats versus tissue cysts from meat), and timing of the infection (eg, in utero, early postnatal, childhood, adulthood). Each of these factors is known to lead to different disease outcomes for other infectious agents. The study of these factors will be important in further defining the relationship between T. gondii and schizophrenia.
Read the article discussion: Forum Discussion: Antibodies to Toxoplasma gondii in Patients with Schizophrenia: A Meta-Analysis
Posted by Jeanie Wolfson at April 18, 2007 06:30 AM
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