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    Zinc, Prenatal LPS and Autism:

    Pregnant-WomanIn order to understand the causes of autistic-like behaviors, researchers from the University of Sao Paulo evaluated maternal serum metal concentrations involved in intra uterine development and infection/inflammation. They identified reduced maternal levels of zinc, magnesium, selenium and manganese after lipopolysaccharide (LPS) exposure in prenatal rats. They selected zinc as the prenatal treatment to prevent or ease the impairments induced by LPS, as cytokines produced after LPS exposure induce metallothionein, which sequesters zinc and induces maternal and fetal hypozincemia. They then treated the dams with zinc in an attempt to prevent or ease the impairments in the offspring, and evaluated the social and cognitive autistic-like behaviors and brain tissues of the offspring to identify the central mechanism that trigger the development of autism. LPS exposure impaired play behaviors and induced autistic-like behaviors. Prenatal LPS also decreased tyrosine hydroxylase levels and increased the levels of mammalian target of rapamycin (mTOR) in the striatum. Thus, striatal dopaminergic impairments may be related to autism. Excessive signaling through the mTOR pathway has been considered a biomarker of autism, corroborating their rat model of autism. Prenatal zinc treatment prevented these autistic-like behaviors and striatal dopaminergic and mTOR disturbances in the offspring induced by LPS exposure. Findings reveal a possible relation between maternal zinc deficiency during gestation and the onset of autism. In this study, prenatal zinc administration demonstrates a beneficial effect on the prevention of autism.

    TB Kirsten, et al. Lipopolysaccharide Exposure Induces Maternal Hypozincemia, and Prenatal Zinc Treatment Prevents Autistic-Like Behaviors and Disturbances in the Striatal Dopaminergic and mTOR Systems of Offspring. PLOS.ONE DOI:10.1371/journal.pone.0134565 July, 28, 2015

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