Toxoplasmosis, but not borreliosis, is associated with psychiatric disorders and symptoms
Schizophrenia Research 2018; 197: 603-604
Toxoplasmosis, but not borreliosis, is associated with psychiatric disorders and symptoms MENTAL
Flegr, J., Horáček, J.
Schizophrenia Research 2018; 197: 603-604
Seroprevalence of Toxoplasma gondii infection in children with central nervous system disorders in Mansoura, Egypt: a case-control study
El-Beshbishi,S. N. , El-Tantawy,N. L, Elzeky, S. M., Abdalaziz , K. F. ,Atia, R. A.
Transactions of the Royal Society of Tropical Medicine and Hygiene 2018;112: 555-560
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Background: Toxoplasma gondii is a global infection with a crucial role in the development of neurological diseases. Data concerning the association between T. gondii and neurological illnesses in Egyptian children is scarce. Methods: A case-control study was conducted on 60 patients divided into children suffering from central nervous system manifestations without apparent chromosomal anomalies (n=30) and children with Down syndrome (n=30) recruited from Mansoura University Children's Hospital, Mansoura, Egypt. A total of 30 healthy children were included as controls. Demographics and clinical data were collected from all cases and Toxoplasma immunoglobulin (Ig) M and G antibodies were assessed by enzyme-linked immunosorbent assay. Results: Anti-T. gondii IgG was the most frequent antibody detected and the highest seropositivity rates were ranked for the neurologically disabled non-syndromic children, followed by Down syndrome, compared with controls (p <= 0.001). Statistically significant (p=0.05) associations were found between Toxoplasma IgG seropositivity and hydrocephalus and between Toxoplasma IgM and a history of contact with farm animals, soil and cats in children with Down syndrome. Conclusions: The association between Toxoplasma infection and neurological disorders in children should be kept in mind by paediatricians and assessment of T. gondii antibodies in early childhood is needed for timely management of afflicted patients.
Prenatal toxoplasmosis antibody and childhood autism
Spann, M. N., Sourander, A., Surcel, H. M., Hinkka-Yli-Salomaki, S., Brown, A. S.
Autism Research 2017; 10: 769-777
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here is evidence that some maternal infections during the prenatal period are associated with neurodevelopmental disorders, such as childhood autism. However, the association between autism and Toxoplasma gondii (T. gondii), an intracellular parasite, remains unclear. The authors examined whether serologically confirmed maternal antibodies to T. gondii are associated with odds of childhood autism in offspring. The study is based on a nested case-control design of a large national birth cohort (N=1.2 million) and the national psychiatric registries in Finland. There were 874 cases of childhood autism and controls matched 1: 1 on date of birth, sex, birthplace and residence in Finland. Maternal sera were prospectively assayed from a national biobank for T. gondii IgM and IgG antibodies; IgG avidity analyses were also performed. High maternal T. gondii IgM antibody was associated with a significantly decreased odds of childhood autism. Low maternal T. gondii IgG antibody was associated with increased offspring odds of autism. In women with high T. gondii IgM antibodies, the IgG avidity was high for both cases and controls, with the exception of three controls. The findings suggest that the relationship between maternal T. gondii antibodies and odds of childhood autism may be related to the immune response to this pathogen or the overall activation of the immune system.
The seroprevalence of antibodies to Toxoplasma gondii among children with autism
Esnafoglu, E., Demir, E.Y., Cetinkol, Y., Calgin, M.K., Erdil, A., Erturk, E.Y., Dagli, A.
Dusunen Adam The Journal of Psychiatry and Neurological Sciences 2017; 30: 309-315
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Objective: Although attempts have been made to explain the pathogenesis of autism spectrum disorders (ASD) with many factors such as genetic, immunological, environmental, and infectious agents, this mechanism remains for the most part unknown. Toxoplasma gondii is a parasite that is investigated in many psychiatric diseases. This work examines whether toxoplasmosis plays a role in the pathogenesis of ASD through a seroprevalence study.
Method: This study is based on a comparison of 102 children with ASD and 51 healthy children. In addition to routine laboratory tests, a sociodemographic form and a childhood autism rating scale were completed and the participants' anti-toxoplasma IgM and IgG titers were requested.
Results: In 3 ASD children (2.9%) and in 1 control (2%), IgG positivity was identified. All subjects were negative for IgM. There was no statistically significant difference found between the two groups in terms of toxoplasma seropositivity.
Conclusion: Our data does not confirm the involvement of toxoplasmosis in the etiopathogenesis of ASD
Maternal infection during pregnancy and risk of autism spectrum disorders: A systematic review and meta-analysis
Jiang, H. Y., Xu, L. L., Shao, L., Xia, R. M., Yu, Z. H., Ling, Z. X., Yang, F., Deng, M., Ruan, B.
Brain Behavior and Immunity 2016; 58: 165-172
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Conflicting evidence exists with regard to the relationship between maternal infection during pregnancy and the risk of autism spectrum disorder (ASD) in offspring. The aim of this meta-analysis was to systematically assess this relationship. To identify relevant studies, we conducted systematic searches in PubMed and Embase of scientific articles published through March 2016. Random-effects models were adopted to estimate overall relative risk. A total of 15 studies (2 cohort and 13 case-control studies) involving more than 40,000 ASD cases were included in our meta-analysis. Our results showed that maternal infection during pregnancy was associated with an increased risk of ASD in offspring (OR = 1.13, 95% confidence interval (CI): 1.03-1.23), particularly among those requiring hospitalization (OR = 1.30, 95% CI: 1.14-1.50). Subgroup analyses suggested that risk may be modulated by the type of infectious agent, time of infectious exposure, and site of infection. These findings indicate that maternal infection during pregnancy increases the risk of ASD in offspring. Possible mechanisms may include direct effects of pathogens and, more indirectly, the effects of inflammatory responses on the developing brain. (C) 2016 Elsevier Inc. All rights reserved.
Gastroenterology issues in schizophrenia: Why the gut matters
Severance, E. G., Prandovszky, E., Castiglione, J., Yolken, R. H.
Current Psychiatry Reports 2015; 17: 10.1007/s11920-015-0574-0
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Genetic and environmental studies implicate immune pathologies in schizophrenia. The body's largest immune organ is the gastrointestinal (GI) tract. Historical associations of GI conditions with mental illnesses predate the introduction of antipsychotics. Cuirent studies of antipsychotic-naive patients support that gut dysfunction may be inherent to the schizophrenia disease process. Risk factors for schizophrenia (inflammation, food intolerances, Toxoplasma gondii exposure, cellular barrier defects) are part of biological pathways that intersect those operant in the gut. Central to GI function is a homeostatic microbial community, and early reports show that it is disrupted in schizophrenia. Bioactive and toxic products derived from digestion and microbial dysbiosis activate adaptive and innate immunity. Complement Clq, a brain-active systemic immune component, interacts with gut-related schizophrenia risk factors in clinical and experimental animal models. With accumulating evidence supporting newly discovered gut brain physiological pathways, treatments to ameliorate brain symptoms of schizophrenia should be supplemented with therapies to correct GI dysfunction.
The “psychomicrobiotic”: Targeting microbiota in major psychiatric disorders: A systematic review
Fond, G., Boukouaci, W., Chevalier, G., Regnault, A., Eberl, G., Hamdani, N., Dickerson, F., Macgregor, A., Boyer, L., Dargel, A., Oliveira, J., Tamouza, R., Leboyer, M.
Pathologie Biologie 2015; 63: 35-42
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The gut microbiota is increasingly considered as a symbiotic partner in the maintenance of good health. Metagenomic approaches could help to discover how the complex gut microbial ecosystem participates in the control of the host's brain development and function, and could be relevant for future therapeutic developments, such as probiotics, prebiotics and nutritional approaches for psychiatric disorders. Previous reviews focused on the effects of microbiota on the central nervous system in in vitro and animal studies. The aim of the present review is to synthetize the current data on the association between microbiota dysbiosis and onset and/or maintenance of major psychiatric disorders, and to explore potential therapeutic opportunities targeting microbiota dysbiosis in psychiatric patients. (C) 2014 Elsevier Masson SAS. All rights reserved.
Are there any relationships between latent Toxoplasma gondii infection, testosterone evelatin, and risk of autism spectrum disorder?
Abdoli A, Dalimi A.
Frontiers in Behavioral Neuroscience 2014; 8
Neuropathological changes and clinical features of autism spectrum disorder participants are similar to that reported in congenital and chronic cerebral toxoplasmosis in humans and mice
Prandota J.
Research in Autism Spectrum Disorders 2010; 4: 103-118.
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Anatomic, histopathologic, and MRI/SPET studies of autistic spectrum disorders (ASD) patients' brains confirm existence of very early developmental deficits. In congenital and chronic murine toxoplasmosis several cerebral anomalies also have been reported, and worldwide, approximately two billion people are chronically infected with T. gondii with largely yet unknown consequences. The aim of the study was therefore to compare brain abnormalities in ASD patients with those found in mice with cerebral toxoplasmosis (CT) because this may help in understanding pathophysiology of ASD. Data from available published studies were analyzed to compare postmortem pathologic changes found in the brains of ASD patients with those of mice developed after intraperitoneal T.gondii infection. Patients with ASD had the following brain abnormalities: active neuroinflammatory process notably in cerebellum, microglial nodules, accumulation of perivascular macrophages, decreased number and size of Purkinje cells in cerebellar nuclei and inferior olive, hypoperfusion of brain. Mice with congenital toxoplasmosis also had persistent neuroinflammation and ventricular enlargement, periventricular edema, meningeal and perivascular inflammation, and focal loss of Purkinje and granule cells. In murine acquired CT, the brain anomalies included: ventricular dilatation probably reflecting loss of brain parenchyma; perivascular inflammation particularly in hippocampus, and periaqueductal/periventricular areas, Purkinje cell layer markedly disfigured with focal loss of cells: perivascular cuffing by mononuclear cells and localized microglial/inflammatory nodules. Infection of mice with different strains of T. gondii resulted in distinctive neuropathological changes and various stadium of maturity of cysts and the parasite itself, which is in line with the diversity of the autistic phenotypes. Also, the abnormalities in behavior and clinical features associated with autism resembled that reported in chronic latent toxoplasmosis in humans and rodents. All these similarities suggest that T gondii should be regarded as an important infectious factor that may trigger development of ASD and some other neurodegenerative diseases, such as obsessive-compulsive and attention-deficit/hyperactivity disorders, and cryptogenic epilepsy. Thus, all these patients should be tested for T. gondii infection. (C) 2009 Elsevier Ltd. All rights reserved.
Autism spectrum disorders may be due to cerebral toxoplasmosis associated with chronic neuroinflammation causing persistent hypercytokinemia that resulted in an increased lipid peroxidation, oxidative stress, and depressed metabolism of endogenous and exogenous substances
Prandota J.
Research in Autism Spectrum Disorders 2010; 4: 119-155
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Worldwide, approximately 2 billion people are chronically infected with Toxoplasma gondii with largely yet unknown consequences. Patients with autism spectrum disorders (ASD) similarly as mice with chronic toxoplasmosis have persistent neuroinflammation, hypercytokinemia with hypermetabolism associated with enhanced lipid peroxidation, and extreme changes in the weight resulting in obesity or wasting. Data presented in this review suggest that environmental triggering factors such as pregnancy, viral/bacterial infections, vaccinations, medications, and other substances caused reactivation of latent cerebral toxoplasmosis because of changes in intensity of latent central nervous system T. gondii infection/inflammation and finally resulted in development of ASD. Examples of such environmental factors together with their respective biomarker abnormalities are: pregnancy (increased NO, IL-1 beta, TNF-alpha, IL-6, IL-10, prolactin: decreased IFN-gamma, IL-12), neuroborreliosis (increased IL-1 beta, sIL-1R2, TNF-alpha, IFN-gamma, IL-6, IL-10, IL-12, IL-18, transforming growth factor-beta 1 (TGF-beta 1)), vital infections (increased IL-1 beta, IL-6, IL-8, TNF-alpha, IFN-gamma/alpha/beta,TGF-beta 1), thimerosal (increased IL-5, IL-13; decreased IFN-gamma,TNF-alpha,IL-6, IL-12p70, NOS), and valproic acid (increased NO, reactive oxygen species; decreased TNF-alpha, IL-6, IFN-gamma). The imbalances in pro- and antiinflammatory processes could markedly hinder [lost defense mechanisms important for immune control of the parasite, such as the production of NO, cytokines, and reactive oxygen/nitrogen species, tryptophan degradation by indoleamine 2,3-dioxygenase and/or tryptophan 2,3-dioxygenase, limitation of the availability of intracellular iron to T gondii, and the mechanisms mediated by an IFN-gamma responsive gene family. These fluctuations could result in a recurrent profuse multiplication of T. gondii in the brain associated with persistent neuroinflammation, chronic overproduction of pro- and antiinflammatory cytokines, and NO causing increased oxidative stress, and significantly depressed activity of several enzymes including cytochrome P450 monooxygenase family responsible for metabolism of physiological substrates and xenobiotics, such as steroids, fatty acids, prostaglandins, drugs, pollutants, and carcinogens, finally leading to development of ASD. This reasoning may be supported by such abnormal metabolic events as: (1) patients with ASD have significantly decreased melatonin levels caused by marked deficit in acetylserotonin methyltransferase activity, possibly resulting from maternal and/or fetal/postnatal overproduction of NO, characteristic for this clinical entity; (2) thimerosal inhibited both insulin-like growth factor-1- and dopamine-stimulated methylation reactions, and depressed methionine synthase activity, the metabolic events important for promoting normal neurodevelopment; (3) valproic acid, a strong histone deacetylase inhibitor, have potent anti-T. gondii activity. Thus, patients with ASD should be tested for T. gondii infection. (C) 2009 Elsevier Ltd. All rights reserved