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    A Proposed Mechanism for Cerebral Toxoplasmosis as a Contributing Factor in Schizophrenia

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    Author
    Pace, Sarah Elise
    Issue Date
    2016
    Keywords
    Mental illness
    parasite
    Schizophrenia
    Toxoplasma gondii
    Toxoplasmosis
    Kynurenic acid
    Advisor
    Krieg, Paul
    
    Metadata
    Show full item record
    Publisher
    The University of Arizona.
    Rights
    Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
    Abstract
    Schizophrenia is a devastating mental disorder that affects around 1% of the world’s population, characterized by the presence of positive symptoms including hallucinations and delusions, negative symptoms including depression and anxiety, and cognitive impairment including deficits in speech and memory. The complete etiology of schizophrenia is not yet understood, though it is known that both genetics and environmental factors play a role. One environmental factor, a chronic cerebral infection by the parasite Toxoplasma gondii, has one of the highest correlations with schizophrenia of any environmental factor, and may play a role in the pathology of the disease. This is especially true in the case of Type I toxoplasma, which is the most virulent of the three common strains of the parasite. Toxoplasmosis causes an increase in dopamine levels in the striatum and substantia nigra through the production of two enzymes that mimic the rate limiting enzyme in dopamine synthesis, tyrosine hydroxylase. Increased dopamine concentrations in these areas are experimentally correlated with positive schizophrenia symptoms. In addition, toxoplasmosis causes chronic upregulation of the kynurenine pathway via INF- release, leading to chronically elevated kynurenic acid levels. This leads to dysfunction of the glutamatergic system via (1) the binding and inhibition ofα7- nicotinic receptors, leading to decreased GABAergic inhibitory activity in the hippocampus and decreased glutamate release in the prefrontal cortex, and (2) NMDA and AMPA receptor hypofunction, causing decreased inhibitory signaling by GABAergic neurons leaving glutamatergic neurons in a hyper-excitable state. These mechanisms, compounded by commonly identified mutations in the genes of schizophrenic individuals affecting the dopaminergic system, the kynurenine pathway,α7-nicotinic receptors, and the glutamatergic system, create a viable theory as to how the interplay between genetics and toxoplasmosis could cause schizophrenia.
    Type
    text
    Electronic Thesis
    Degree Name
    M.S.
    Degree Level
    masters
    Degree Program
    Graduate College
    Cellular and Molecular Medicine
    Degree Grantor
    University of Arizona
    Collections
    Master's Theses

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