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Query: UMLS:C0036341 (schizophrenia)
 60,220 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Toxoplasma gondii, a parasitic protozoan, infects about 30-60% of people worldwide. The latent toxoplasmosis, i.e. life-long presence of cysts in the brain and muscular tissues, has no effect on human health. However, infected subjects score worse in psychomotor performance tests and have different personality profiles than Toxoplasma-negative subjects. The mechanism of this effect is unknown; however, it is supposed that presence of parasites' cysts in the brain induces an increase of the concentration of dopamine. Here we search for the existence of differences in personality profile between Toxoplasma-positive and Toxoplasma-negative subjects by testing 857 military conscripts using a modern psychobiological questionnaire, namely with Cloninger's Temperament and Character Inventory (TCI). ANCOVA showed that Toxoplasma-positive subjects had lower Novelty seeking (NS) scores (P=0.035) and lower scores for three of its four subscales, namely Impulsiveness (P=0.049), Extravagance (P=0.056) and Disorderliness (P=0.006) than the Toxoplasma-negative subjects. Differences between Toxoplasma-negative and positive subjects in NS was inversely correlated with duration of toxoplasmosis estimated on the basis of concentration anti-Toxoplasma antibodies (P=0.031). Unexpectedly, the infected subjects had also lower IQ (P(2)=0.003) and lower probability of achieving a higher education (P(2)<0.0000). Decrease of NS suggests that the increase of dopamine in brain of infected subjects can represent a missing link between toxoplasmosis and schizophrenia.
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PMID:Decreased level of psychobiological factor novelty seeking and lower intelligence in men latently infected with the protozoan parasite Toxoplasma gondii Dopamine, a missing link between schizophrenia and toxoplasmosis? 1285 70

One of the most compelling topics to emerge from the last decade of veterinary protozoology is disease caused by a zoonotic pathogen, Toxoplasma gondii, in otherwise healthy people. These findings may catch the health professions by surprise, because veterinary and medical courses and textbooks typically emphasize that T. gondii infections are subclinical, unless acquired in utero or the patient has a serious immunosuppressive condition. Nevertheless, numerous reports in the last decade associate toxoplasmosis with lymphadenopathy, fever, weakness and debilitation, ophthalmitis, and severe multisystemic infections in people who do not have immunosuppressive conditions. Toxoplasmosis in rodents causes altered behavior, and similar mental aberrations are coming to light in humans; recent studies associate T. gondii infection with personality shifts and increased likelihood of reduced intelligence or schizophrenia. These conditions reduce the quality of life of individuals, and may exact a significant economic burden upon society. Of course, toxoplasmosis continues to cause serious conditions in AIDS patients and congenitally infected people, as well as abortions and encephalitis in domestic and wild animals. Environmental contamination is heavy enough to extend into marine wildlife. It is time for the health professions to amend teaching curricula regarding T. gondii. Veterinary parasitologists should lead the way in developing methods to reduce the prevalence of T. gondii in food animals. Public health policies should prohibit the practice of allowing pet cats to roam. Organizations and individuals that feed feral cats are unwittingly contributing to the dissemination of T. gondii, by sustaining artificially dense populations of a definitive host of this protozoal parasite.
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PMID:A decade of discoveries in veterinary protozoology changes our concept of "subclinical" toxoplasmosis. 1609 40

Accumulating evidence suggests that prenatal exposure to infection contributes to the etiology of schizophrenia. This line of investigation has been advanced by birth cohort studies that utilize prospectively acquired data from serologic assays for infectious and immune biomarkers. These investigations have provided further support for this hypothesis and permitted the investigation of new infectious pathogens in relation to schizophrenia risk. Prenatal infections that have been associated with schizophrenia include rubella, influenza, and toxoplasmosis. Maternal cytokines, including interleukin-8, are also significantly increased in pregnancies giving rise to schizophrenia cases. Although replication of these findings is required, this body of work may ultimately have important implications for the prevention of schizophrenia, the elaboration of pathogenic mechanisms in this disorder, and investigations of gene-environment interactions.
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PMID:Prenatal infection as a risk factor for schizophrenia. 1646 41

The infection of humans with opportunistic protozoon Toxoplasma gondii is severe for immunocompromised individuals (AIDS patients, transplant recipients, fetuses). Because of the lack of protective vaccines, the rules of primary (avoidance) prevention have to be introduced. The principles of such prevention, particularly important for seronegative pregnant women, as well as new data on the possibility of T. gondii reinfection in seropositive humans and animals were presented in the article. The attention was also focused on laboratory diagnostics of toxoplasmosis, associated, among others, with prolonged persistence of specific IgM antibodies and delayed maturation of IgG antibodies. The psychic and physical consequences of chronic Toxoplasma gondii infections were mentioned (lowered IQ, schizophrenia etc.).
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PMID:[Aspects of diagnostics and prevention of toxoplasmosis]. 1688 55

Schizophrenia is a serious neuropsychiatric disease of uncertain etiology. We investigated the seropositivity rate for anti-Toxoplasma IgG and IgM antibodies by enzyme-linked immunosorbent assay (ELISA) in patients with schizophrenia to ascertain a possible relationship between Toxoplasma gondii and schizophrenia. We selected 100 patients with schizophrenia, 50 with depressive disorder, and 50 healthy volunteers to investigate the seropositivity rate of anti-Toxoplasma antibodies by ELISA. The seropositivity rate for anti-Toxoplasma IgG antibodies among schizophrenia patients (66%) was significantly higher than among patients with depressive disorder or healthy volunteers (P < .01). Thus, there might be a causal relationship between toxoplasmosis and the etiology of schizophrenia.
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PMID:Anti-Toxoplasma gondii antibodies in patients with schizophrenia--preliminary findings in a Turkish sample. 1740 88

In recent years, the effect of Toxoplasma gondii infection on psychiatric-related aspects has been increasingly recognized. T. gondii has a high affinity for brain tissue where tachyzoites may form tissue cysts and persist life long. In recent years, 15 serological surveys about T. gondii infection and psychiatric diseases have been carried out in different areas in China. Studies showed that the prevalence of antibodies against T. gondii in psychotic patients was much higher than in normal persons; statistically differences were significant. Studies also reported that raising cats or enjoying the habit of eating raw or under cooked meet were potential risk factors for the infection of T. gondii. The epidemiological and serological evidence support the hypothesis that some psychiatric diseases such as schizophrenia or mental retardation might be linked to T. gondii infection.
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PMID:Epidemiological evidences from China assume that psychiatric-related diseases may be associated with Toxoplasma gondii infection. 1743 77

Recent meta-analyses have provided a comprehensive overview of studies investigating Toxoplasma gondii antibodies in schizophrenic patients, thus attempting to clarify the potential role these infections might play in causing schizophrenia. Issues for further research have been suggested. Associations and theories that may enrich the current level of knowledge with regard to this significant subject deserve attention. Anti-parasitic agents as well as antipsychotics are effective in treating parasitosis. Both classes of drugs have been shown to exert dopaminergic activity. Parasites and human organisms have a long history of mutual contact. The effect of parasitosis on the host and the host's response to infection are undoubtedly the product of a long evolutionary process. The neurochemical background of delusions of parasitosis is potentially similar to ancient evolutionary traces of altered neurotransmission and neuropeptide gene expression caused by parasites; these include fungal and viral infections. This is very unique in medicine if a class of drugs is effective in the treatment of an illness but also cures the delusion of the same disorder as well. Furthermore, metabolic disturbances such as hyperglycemia and insulin resistance were reported several decades before the antipsychotic era. Toxoplasmosis may also be linked to insulin resistance. Schizophrenia research can benefit from understanding this evolutionary link. New chemical entities that are liable to alter neurochemical changes related to the brain's perception of the risk of predation secondary to parasites may result in new approaches for the treatment of psychosis. These findings suggest that further research is needed to clarify this evolutionary link between parasite infection and delusions of parasitosis. We believe this model may well open up new avenues of research in the discovery of drugs to counteract schizophrenia.
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PMID:Parasitosis, dopaminergic modulation and metabolic disturbances in schizophrenia: evolution of a hypothesis. 1798 33

Toxoplasma gondii is a common intracellular protozoan infection of humans worldwide. Severe disease can occur in immunocompromised individuals and the in the fetuses of nonimmune pregnant women. Chronic infection is associated with vision and hearing problems, and functional mental alterations, including schizophrenia. The mood-stabilizing agent valproic acid has been shown to inhibit the development of T. gondii in vitro at dosages that are normally achieved in the serum and cerebral spinal fluid of human patients and to have positive effects on the behavior of rats chronically infected with T. gondii. The present study was done to examine the in vivo activity of valproic acid against acute toxoplasmosis in mice. Two studies were done with valproic acid given in the drinking water at concentrations of 1.5 mg/ml (Experiment 1) or 3.0 mg/ml (Experiment 2). In a third experiment (Experiment 3), valproic acid was injected intraperitoneally (i.p.) at doses of 200 or 300 mg/kg every 12 hr. Valproic acid was not effective in preventing acute toxoplasmosis. All mice treated with valproic acid died or were killed and did not (P > 0.05) live significantly longer than the controls. Tachyzoites were demonstrated in the tissues of infected valproic-acid-treated mice. A fourth study was done to determine if valproic acid has activity against T. gondii tissue cysts in chronically infected mice. Mice were chronically infected with the ME-49 strain of T. gondii for 8 wk and then treated orally with valproic acid at approximately 6.6 mg/ml (800 mg/kg/day) in the drinking water for 10 wk (amount was varied due to increasing mouse weights). No significant differences (P > 0.05) were present in tissue cyst numbers in valproic-acid-treated T. gondii chronically infected mice and in mice chronically infected with T. gondii but not given valproic acid. Our results indicate that valproic acid, although effective in vitro against T. gondii tachyzoites, is not effective as a preventative in mice inoculated with T. gondii tachyzoites. Additionally, no activity against tissue cysts was observed in chronically T. gondii-infected valproic-acid-treated mice.
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PMID:Evaluation of the mood-stabilizing agent valproic acid as a preventative for toxoplasmosis in mice and activity against tissue cysts in mice. 1856 64

Now that schizophrenia researchers may be moving from unilateral molecular genetic approaches to models including so-called gene-environment interactions, the question rises which environments may be considered for such research and how a user perspective may inform the field. It is argued that trauma and stigma, or perhaps better structural discrimination, represent 2 important environmental factors that deserve more attention. Experiential evidence, collected by users, suggests that trauma in childhood and/or adulthood, before, during, and after the onset of schizophrenia, as well as stigma/structural discrimination, may play important roles in the onset and course of the disorder. A certain reluctance on the part of the professional schizophrenia research community to take these variables as serious as, eg, interesting but inconclusive etiological signals from prenatal hypoxia, prenatal folate deficiency, and prenatal toxoplasmosis is suggested. This article outlines the concepts of trauma and stigma and their negative consequences for the onset and course of schizophrenia. The importance of research into these factors and their possible relevance for gene-environment interactions is discussed. While gene-environment interaction research using these variables is indicated and may possibly prove productive, it is argued that such efforts may not be useful if no subsequent attempt is made to translate the results to the level of interventions, codeveloped by users, eg, in the area of coping with the vicious circle of environmental adversity that users can become exposed to.
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PMID:Which environments for G x E? A user perspective on the roles of trauma and structural discrimination in the onset and course of schizophrenia. 1879 Oct 78

Various infectious agents, such as Toxoplasma gondii, have been hypothesized to be potentially relevant etiological factors in the onset of some cases of schizophrenia. We conducted a randomized, double-blind, placebo-controlled treatment trial in an attempt to explore the hypothesis that the symptoms of schizophrenia may be related to infection of the central nervous system with toxoplasma gondii. Systematically selected patients with ongoing and at least moderately severe schizophrenia from Butajira, in rural Ethiopia, were randomly allocated to trimethoprim or placebo, which were added on to participants' regular antipsychotic treatments. Trial treatments were given for 6 months. The Positive and Negative Syndrome Scale (PANSS) was used to assess outcome. Ninety-one patients were included in the study, with 80 cases (87.9%) positive for T. gondii immunoglobulin G antibody. Seventy-nine subjects (87.0%) completed the trial. The mean age of subjects was 35.3 (SD = 8.0) years, with a mean duration of illness of 13.2 (SD = 6.7) years. Both treatment groups showed significant reduction in the overall PANSS score with no significant between-group difference. In this sample of patients with chronic schizophrenia, trimethoprim used as adjuvant treatment is not superior to placebo. However, it is not possible to draw firm conclusion regarding the etiological role of toxoplasmosis on schizophrenia based on this study because the timing and the postulated mechanisms through which toxoplasmosis produces schizophrenia are variable.
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PMID:Trimethoprim as adjuvant treatment in schizophrenia: a double-blind, randomized, placebo-controlled clinical trial. 1919 43


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