![]() Maternal IgG isotype antibodies cross the placenta beginning by week 17 of gestation to equip the immunologically naïve fetus with a subset of antibodies that provide protection against a myriad of possible infectious agents. ![]() These alterations are produced by prenatal and postnatal changes in the normal patterns of cortical development, including stem cell function and neurite outgrowth. Neuropathological changes in affected brain areas include alterations in cell numbers and connectivity. ![]() Identified regions of the brain that are affected in ASD include the cerebral cortex and the cerebellum. Recent estimates indicate that 1 in 68 children in the United States are impacted by ASD. NICHD funded IDDRC 054 (U54HD079125).Ĭompeting interests: The authors have declared that no competing interests exist.Īutism spectrum disorders (ASD) are defined by a pattern of qualitative abnormalities in reciprocal social interaction, communication, and repetitive interests and behaviors. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.ĭata Availability: Data are all contained within the paperįunding: Funded by NIMH, MH094681 to VMC, Shiners Hospitals to VMC, NIEHS Center for Children’s Environmental Health 2P01ES011269-11 to JVW, Environmental Protection Agency (EPA), 8354320 to JVW. ![]() Received: JanuAccepted: AugPublished: August 18, 2017Ĭopyright: © 2017 Ariza et al. PLoS ONE 12(8):Įditor: Alexandre Hiroaki Kihara, Universidade Federal do ABC, BRAZIL (2017) Maternal autoimmune antibodies alter the dendritic arbor and spine numbers in the infragranular layers of the cortex. Here we hypothesize that the reduction in the access of newborn cells to STIP1 in the developing cortex may be responsible for the reduced dendritic arborization and number of spines we noted in the adult cortex.Ĭitation: Ariza J, Hurtado J, Rogers H, Ikeda R, Dill M, Steward C, et al. We recently demonstrated that one of the primary antigens recognized by these antibodies corresponds to stress-induced phosphoprotein 1 (STIP1). Interestingly, the time of exposure to these antibodies (E14.5) coincides with the generation of pyramidal neurons in layer V in the frontal cortex and in layer VI in the occipital cortex, following the normal rostro-caudal pattern of cortical cell generation. Further, in the occipital cortex layer VI neurons presented with a decrease in the total number of spines and in the spine density in the apical dendrite, as well as decrease in the number of mature spines in the apical and basal dendrites. Specifically, in the frontal cortex basal dendrites of layer V neurons were decreased in length and volume, and both the total number of spines-mature and immature-and the spine density were lower than in the control neurons from the same region. Here, we used our intraventricular mouse model of antibody administration, followed by Golgi and Neurolucida analysis to demonstrate that during midstages of neurogenesis these maternal autism-specific antibodies produced a consistent decrease in the number of spines in the infragranular layers in the adult cortical areas analyzed. We also showed an alteration in brain size and as well as a generalized increased of neuronal volume in adult mice. We previously demonstrated that these antibodies bind to radial glial stem cells (RG) and observed an increase in the number of divisions of translocating RG in the developing cortex. Using a mouse model of prenatal intraventricular administration of autism-specific maternal IgG, we demonstrated that these antibodies produce behavioral alterations similar to those in children with ASD. An association between maternal IgG antibodies reactive against proteins in fetal brain and an outcome of autism in the child has been identified.
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