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Neuropsychiatric disease and Toxoplasma gondii infection.

Abstract

Toxoplasma gondii infects approximately 30% of the world's population, but causes overt clinical symptoms in only a small proportion of people. In recent years, the ability of the parasite to manipulate the behaviour of infected mice and rats and alter personality attributes of humans has been reported. Furthermore, a number of studies have now suggested T. gondii infection as a risk factor for the development of schizophrenia and depression in humans. As T. gondii forms cysts that are located in various anatomical sites including the brain during a chronic infection, it is well placed anatomically to mediate these effects directly. The T. gondii genome is known to contain 2 aromatic amino acid hydroxylases that potentially could directly affect dopamine and/or serotonin biosynthesis. However, stimulation of the immune response has also recently been associated with mood and behavioural alterations in humans, and compounds designed to alter mood, such as fluoxetine, have been demonstrated to alter aspects of immune function. Herein, the evidence for T.-gondii-induced behavioural changes relevant to schizophrenia and depression is reviewed. Potential mechanisms responsible for these changes in behaviour including the role of tryptophan metabolism and the hypothalamic-pituitary-adrenal axis are discussed.

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  • Authors+Show Affiliations

    ,

    Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, 27 Taylor Street, Glasgow, UK.

    , , ,

    Source

    Neuroimmunomodulation 16:2 2009 pg 122-33

    MeSH

    Animals
    Behavior
    Behavior, Animal
    Cats
    Cytokines
    Depression
    Dopamine
    Female
    Host-Parasite Interactions
    Humans
    Male
    Mental Disorders
    Mice
    Nervous System Diseases
    Neurons
    Neurosecretory Systems
    Protozoan Proteins
    Rats
    Risk Factors
    Schizophrenia
    Serotonin
    Toxoplasma
    Toxoplasmosis
    Toxoplasmosis, Animal
    Tryptophan

    Pub Type(s)

    Journal Article
    Review

    Language

    eng

    PubMed ID

    19212132

    Citation

    Henriquez, S A., et al. "Neuropsychiatric Disease and Toxoplasma Gondii Infection." Neuroimmunomodulation, vol. 16, no. 2, 2009, pp. 122-33.
    Henriquez SA, Brett R, Alexander J, et al. Neuropsychiatric disease and Toxoplasma gondii infection. Neuroimmunomodulation. 2009;16(2):122-33.
    Henriquez, S. A., Brett, R., Alexander, J., Pratt, J., & Roberts, C. W. (2009). Neuropsychiatric disease and Toxoplasma gondii infection. Neuroimmunomodulation, 16(2), pp. 122-33. doi:10.1159/000180267.
    Henriquez SA, et al. Neuropsychiatric Disease and Toxoplasma Gondii Infection. Neuroimmunomodulation. 2009;16(2):122-33. PubMed PMID: 19212132.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Neuropsychiatric disease and Toxoplasma gondii infection. AU - Henriquez,S A, AU - Brett,R, AU - Alexander,J, AU - Pratt,J, AU - Roberts,C W, Y1 - 2009/02/11/ PY - 2009/2/13/entrez PY - 2009/2/13/pubmed PY - 2009/6/20/medline SP - 122 EP - 33 JF - Neuroimmunomodulation JO - Neuroimmunomodulation VL - 16 IS - 2 N2 - Toxoplasma gondii infects approximately 30% of the world's population, but causes overt clinical symptoms in only a small proportion of people. In recent years, the ability of the parasite to manipulate the behaviour of infected mice and rats and alter personality attributes of humans has been reported. Furthermore, a number of studies have now suggested T. gondii infection as a risk factor for the development of schizophrenia and depression in humans. As T. gondii forms cysts that are located in various anatomical sites including the brain during a chronic infection, it is well placed anatomically to mediate these effects directly. The T. gondii genome is known to contain 2 aromatic amino acid hydroxylases that potentially could directly affect dopamine and/or serotonin biosynthesis. However, stimulation of the immune response has also recently been associated with mood and behavioural alterations in humans, and compounds designed to alter mood, such as fluoxetine, have been demonstrated to alter aspects of immune function. Herein, the evidence for T.-gondii-induced behavioural changes relevant to schizophrenia and depression is reviewed. Potential mechanisms responsible for these changes in behaviour including the role of tryptophan metabolism and the hypothalamic-pituitary-adrenal axis are discussed. SN - 1423-0216 UR - https://www.unboundmedicine.com/medline/citation/19212132/Neuropsychiatric_disease_and_Toxoplasma_gondii_infection_ L2 - https://www.karger.com?DOI=10.1159/000180267 DB - PRIME DP - Unbound Medicine ER -