Schizophrenia: Prenatal Influenza and Autoimmunity

Wright, Pádraig; Murray, Robin M.

doi:10.3109/07853899309147318

Cited by 42 publications

(21 citation statements)

References 64 publications

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“…This is similar to the finding of hippocampal pyramidal cell disarray reported in human schizophrenia post-mortem studies [138][139][140] . Because the influenza virus or influenza virus antibodies have not been detected in the fetal brain, it has been hypothesized that the maternal immune response alone is sufficient to generate schizophrenia-like behavioural findings in the offspring 136,[141][142][143][144][145] . At the neurotransmitter level, dysfunctions in the dopaminergic and glutamatergic system have been reported, especially in the medial prefrontal cortex and the nucleus accumbens in offspring from mothers subjected to immune challenge 123 .…”

Section: Maternal Immune Activationmentioning

confidence: 99%

Estudos traducionais de neuropsiquiatria e esquizofrenia: modelos animais genéticos e de neurodesenvolvimento

Gottschalk

Sarnyai

Guest

et al. 2012

Arch. Clin. Psychiatry (São Paulo)

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Psychiatric symptoms are subjective by nature and tend to overlap between different disorders. The modelling of a neuropsychiatric disorder therefore faces challenges because of missing knowledge of the fundamental pathophysiology and a lack of accurate diagnostics. Animal models are used to test hypotheses of aetiology and to represent the human condition as close as possible to increase our understanding of the disease and to evaluate new targets for drug discovery. In this review, genetic and neurodevelopmental animal models of schizophrenia are discussed with respect to behavioural and neurophysiological findings and their association with the clinical condition. Only specific animal models of schizophrenia may ultimately lead to novel diagnostic approaches and drug discovery. We argue that molecular biomarkers are important to improve animal to human translation since behavioural readouts lack the necessary specificity and reliability to assess human psychiatric symptoms.Gottschalk MG, et al. / Rev Psiq Clín. 2013;40(1):41-50 Keywords: Translational research, neuropsychiatry, genetic, neurodevelopment, animal model, schizophrenia. ResumoSintomas psiquiátricos são subjetivos por natureza e tendem a se sobrepor entre diferentes desordens. Sendo assim, a criação de modelos de uma desordem neuropsiquiátrica encontra desafios pela falta de conhecimento dos fundamentos da fisiopatologia e diagnósticos precisos. Modelos animais são usados para testar hipóteses de etiologia e para representar a condição humana tão próximo quanto possível para aumentar nosso entendimento da doença e avaliar novos alvos para a descoberta de drogas. Nesta revisão, modelos animais genéticos e de neurodesenvolvimento de esquizofrenia são discutidos com respeito a achados comportamentais e neurofisiológicos e sua associação com a condição clínica. Somente modelos animais específicos de esquizofrenia podem, em último caso, levar a novas abordagens diagnósticas e descoberta de drogas. Argumentamos que biomarcadores moleculares são importantes para aumentar a tradução de animais a humanos, já que faltam a especificidade e a fidelidade necessárias às leituras comportamentais para avaliar sintomas psiquiátricos humanos.Gottschalk MG, et al. / Rev Psiq Clín. 2013;40(1):41-50

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Section: Maternal Immune Activationmentioning

confidence: 99%

Estudos traducionais de neuropsiquiatria e esquizofrenia: modelos animais genéticos e de neurodesenvolvimento

Gottschalk

Sarnyai

Guest

et al. 2012

Arch. Clin. Psychiatry (São Paulo)

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“…Other factors associated with increased schizophrenic births include famine during pregnancy, 63,64 Rh factor incompatibility, 65 and autoimmunity due to infectious agents. 66 A number of animal models are currently in use to study schizophrenia and identify potential new therapies (reviewed by Carpenter and Koenig 7 ). Our laboratory has studied the effects of prenatal human influenza viral infection on day 9 of pregnancy in BALB/c and C57BL/6 mice and their offspring.…”

Section: Environmental Factorsmentioning

confidence: 99%

The Neurodevelopmental Hypothesis of Schizophrenia, Revisited

Fatemi

Folsom²

2009

Schizophrenia Bulletin

709

460

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While multiple theories have been put forth regarding the origin of schizophrenia, by far the vast majority of evidence points to the neurodevelopmental model in which developmental insults as early as late first or early second trimester lead to the activation of pathologic neural circuits during adolescence or young adulthood leading to the emergence of positive or negative symptoms. In this report, we examine the evidence from brain pathology (enlargement of the cerebroventricular system, changes in gray and white matters, and abnormal laminar organization), genetics (changes in the normal expression of proteins that are involved in early migration of neurons and glia, cell proliferation, axonal outgrowth, synaptogenesis, and apoptosis), environmental factors (increased frequency of obstetric complications and increased rates of schizophrenic births due to prenatal viral or bacterial infections), and gene-environmental interactions (a disproportionate number of schizophrenia candidate genes are regulated by hypoxia, microdeletions and microduplications, the overrepresentation of pathogen-related genes among schizophrenia candidate genes) in support of the neurodevelopmental model. We relate the neurodevelopmental model to a number of findings about schizophrenia. Finally, we also examine alternate explanations of the origin of schizophrenia including the neurodegenerative model.

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“…Since viral infections are more common in winter, the disturbance of the intrauterine environment by maternal viral infection was supposed to explain the excess of winter births in schizophrenia, restoring an old hypothesis on the viral origin of insanity [44,45]. A slim majority of studies effectively reported an association between maternal exposition to influenza or other viral infections (namely polio, herpes, CMV, rubella) and subsequent diagnosis of schizophrenia in the offspring [24,[46][47][48][49][50].…”

Section: Perinatal Complications and Schizophreniamentioning

confidence: 97%

Genetics, Perinatal Insult and Schizophrenia: The Mechanism Underlying an Increased Prevalence of Perinatal Complications Among Individuals with a Diagnosis of Schizophrenia?

Preti¹,

Miotto²

2005

CPSR

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Recent studies on animals and humans point to the possibility that environmental events might impact on genetic predisposition to abnormal reactions after CNS lesion, causing deviations in the natural course of brain maturation that may result in neuropsychiatric disorders.The literature on the genetic basis of obstetric complications risk is here summarized and linked to the large body of studies indicating perinatal and prenatal adverse events as significant antecedents of schizophrenia.The hypothesis of an important link between obstetric complications on a genetic basis and the risk of schizophrenia is put forward, with an illustration of the studies that will allow accepting or rejecting the proposed hypothesis.

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Schizophrenia: Prenatal Influenza and Autoimmunity

Cited by 42 publications

References 64 publications

Estudos traducionais de neuropsiquiatria e esquizofrenia: modelos animais genéticos e de neurodesenvolvimento

Estudos traducionais de neuropsiquiatria e esquizofrenia: modelos animais genéticos e de neurodesenvolvimento

The Neurodevelopmental Hypothesis of Schizophrenia, Revisited

Genetics, Perinatal Insult and Schizophrenia: The Mechanism Underlying an Increased Prevalence of Perinatal Complications Among Individuals with a Diagnosis of Schizophrenia?

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