Multiple pathways in prevention of immune-mediated brain disorders: Implications for the prevention of autism

Fatemi, S. Hossein

doi:10.1016/j.jneuroim.2009.09.011

Cited by 7 publications

(6 citation statements)

References 42 publications

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“…JAK2, which is dysregulated in ASD and its multiple immune-related co-morbidities, regulates STAT3 activity, which in turn transduces interleukin-6 (IL-6) signals. Increased IL-6 in the maternal serum has been known to alter fetal brain development, impairing social behaviors in the offspring [48, 49]. The alpha and beta subunits of G-proteins, dysregulated in ASD, asthma, IBD, and bacterial and viral infections, are important signaling molecules, which are often considered to have weak links to a number of brain conditions.…”

Section: Resultsmentioning

confidence: 99%

Integrative analysis of genetic data sets reveals a shared innate immune component in autism spectrum disorder and its co-morbidities

et al. 2016

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BackgroundAutism spectrum disorder (ASD) is a common neurodevelopmental disorder that tends to co-occur with other diseases, including asthma, inflammatory bowel disease, infections, cerebral palsy, dilated cardiomyopathy, muscular dystrophy, and schizophrenia. However, the molecular basis of this co-occurrence, and whether it is due to a shared component that influences both pathophysiology and environmental triggering of illness, has not been elucidated. To address this, we deploy a three-tiered transcriptomic meta-analysis that functions at the gene, pathway, and disease levels across ASD and its co-morbidities.ResultsOur analysis reveals a novel shared innate immune component between ASD and all but three of its co-morbidities that were examined. In particular, we find that the Toll-like receptor signaling and the chemokine signaling pathways, which are key pathways in the innate immune response, have the highest shared statistical significance. Moreover, the disease genes that overlap these two innate immunity pathways can be used to classify the cases of ASD and its co-morbidities vs. controls with at least 70 % accuracy.ConclusionsThis finding suggests that a neuropsychiatric condition and the majority of its non-brain-related co-morbidities share a dysregulated signal that serves as not only a common genetic basis for the diseases but also as a link to environmental triggers. It also raises the possibility that treatment and/or prophylaxis used for disorders of innate immunity may be successfully used for ASD patients with immune-related phenotypes.Electronic supplementary materialThe online version of this article (doi:10.1186/s13059-016-1084-z) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Integrative analysis of genetic data sets reveals a shared innate immune component in autism spectrum disorder and its co-morbidities

et al. 2016

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“…Medicinal plants containing bioactive compounds such as polyphenols, flavonoids, saponins, glucosides, and alkaloids have also been shown to disturb viral propagation (reviewed in Wang et al, 2006). More specifically, flavonoids have been demonstrated to exert an anti-influenza effect (Parker-Athill et al, 2009; Fatemi, 2009; Liu et al, 2008; Nagai et al, 1995). …”

Section: Preventive Measures and Therapeutic Interventionsmentioning

confidence: 99%

Viral infection, inflammation and schizophrenia

Kneeland

Fatemi

2013

Progress in Neuro-Psychopharmacology and Biological Psychiatry

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133

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Schizophrenia is a severe neurodevelopmental disorder with genetic and environmental etiologies. Prenatal viral/bacterial infections and inflammation play major roles in the genesis of schizophrenia. In this review, we describe a viral model of schizophrenia tested in mice whereby the offspring of mice prenatally infected with influenza at E7, E9, E16, and E18 show significant gene, protein, and brain structural abnormalities postnatally. Similarly, we describe data on rodents exposed to bacterial infection or injected with a synthetic viral mimic (PolyI:C) also demonstrating brain structural and behavioral abnormalities. Moreover, human serologic data has been indispensible in supporting the viral theory of schizophrenia. Individuals born seropositive for bacterial and viral agents are at a significantly elevated risk of developing schizophrenia. While the specific mechanisms of prenatal viral/bacterial infections and brain disorder are unclear, recent findings suggest that the maternal inflammatory response may be associated with fetal brain injury. Preventive and therapeutic treatment options are also proposed. This review presents data related to epidemiology, human serology, and experimental animal models which support the viral model of schizophrenia.

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“…In a 2007 issue of Science, Patterson hypothesized that by far the most important environmental risks for autism and schizophrenia consist of intrauterine infection before birth [3]. Fatemi, in 2009, mentions the same: that based on major agreement and several decades of studies, maternal infection is responsible, leading toward autism and schizophrenia [4]. The evidence for mental illness, including autism and schizophrenia, being the result of an infectious disease is quite extensive.…”

Section: Discussionmentioning

confidence: 99%

The Science Behind Autism and the 'Developmental Disorders': Tortuous or Tortured?

Broxmeyer¹

2017

GJIDD

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California, in 1999, had been on high alert for some time. Level one autism, without any of its "spectrum," went from almost five thousand cases in late summer 1993 to an estimated 20,377 cases by December 2002. As California's Department of Developmental Services stood by incredulously, it witnessed a tripling of California's autism rate, and all but 15 percent of cases were in children.California wasn't alone. But its autism rates had become the fastest growing group in that state's developmental disability system, and a number of Bay Area school districts were forced to fill entire classes with youths with different forms of autism.But even in the midst of California's mini-epidemic, its Santa Clara County seemed particularly singled out. The Department of Social Services Aid, brokered by the San Andreas Regional Center, staggered to its breaking point, and its forecast for autism in Santa Clara wasn't good.

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Multiple pathways in prevention of immune-mediated brain disorders: Implications for the prevention of autism

Cited by 7 publications

References 42 publications

Integrative analysis of genetic data sets reveals a shared innate immune component in autism spectrum disorder and its co-morbidities

Integrative analysis of genetic data sets reveals a shared innate immune component in autism spectrum disorder and its co-morbidities

Viral infection, inflammation and schizophrenia

The Science Behind Autism and the 'Developmental Disorders': Tortuous or Tortured?

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