Autism spectrum disorder and maternal immune activation: Environmental factors during pregnancy, such as infections, maternal stress or autoimmune disorders, are closely associated with the prevalence of neurodevelopm...Autism spectrum disorder and maternal immune activation: Environmental factors during pregnancy, such as infections, maternal stress or autoimmune disorders, are closely associated with the prevalence of neurodevelopmental disorders including autism spectrum disorder(ASD), bipolar disorder and schizophrenia.It has been shown that severe infections during pregnancy cause maternal immune activation(MIA) and significantly increase the risk of ASD in the offspring although the mechanisms are poorly understood.Many rodent MIA studies support this causal link by showing that offspring of dams administered with polyinosinic:polycytidylic acid(poly I:C), a viral mimetic Toll-like receptor 3 agonist, exhibit longlasting ASD-like behavioral abnormalities such as increased repetitive behavior, impaired social interaction and communication.Interestingly, MIA alters inflammatory cytokine expressions persisting through development and adulthood in the brain of the offspring, suggesting that chronic neuroimmune dysfunction plays a role in mediating the deleterious effects of MIA on neurodevelopment(Garay et al., 2013).展开更多
基金funded in part by Nancy Lurie Marks Family Foundation (to SI)Robert E.Landreth and Dona Landreth Family Foundation (to SI)NIH 5P30 AG013846-23 (to SI)。
文摘Autism spectrum disorder and maternal immune activation: Environmental factors during pregnancy, such as infections, maternal stress or autoimmune disorders, are closely associated with the prevalence of neurodevelopmental disorders including autism spectrum disorder(ASD), bipolar disorder and schizophrenia.It has been shown that severe infections during pregnancy cause maternal immune activation(MIA) and significantly increase the risk of ASD in the offspring although the mechanisms are poorly understood.Many rodent MIA studies support this causal link by showing that offspring of dams administered with polyinosinic:polycytidylic acid(poly I:C), a viral mimetic Toll-like receptor 3 agonist, exhibit longlasting ASD-like behavioral abnormalities such as increased repetitive behavior, impaired social interaction and communication.Interestingly, MIA alters inflammatory cytokine expressions persisting through development and adulthood in the brain of the offspring, suggesting that chronic neuroimmune dysfunction plays a role in mediating the deleterious effects of MIA on neurodevelopment(Garay et al., 2013).
