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10.1007/s00401-017-1751-5 http://scihub22266oqcxt.onion/10.1007/s00401-017-1751-5 C5587616!5587616 !28755208     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28755208 &cmd=llinks): Failed to open stream: HTTP request failed! 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Persistent microglial activation and synaptic loss with behavioral abnormalities in mouse offspring exposed to CASPR2-antibodies in utero |pdf=|usr=}}{{28755208 }} gab.com Text Persistent microglial activation and synaptic loss with behavioral abnormalities in mouse offspring exposed to CASPR2-antibodies in utero JO: Acta Neuropathol http://www.kidney.de/pget.php?&tw=1&pmid=28755208 #FOAvip Gestational transfer of maternal antibodies against fetal neuronal proteins may be relevant to some neurodevelopmental disorders, but until recently there were no proteins identified. We recently reported a fivefold increase in CASPR2-antibodies in mid-gestation sera from mothers of children with intellectual and motor disabilities. Here, we exposed mice in utero to purified IgG from patients with CASPR2-antibodies (CASPR2-IgGs) or from healthy controls (HC-IgGs). CASPR2-IgG but not HC-IgG bound to fetal brain parenchyma, from which CASPR2-antibodies could be eluted. CASPR2-IgG exposed neonates achieved milestones similarly to HC-IgG exposed controls but, when adult, the CASPR2-IgG exposed progeny showed marked social interaction deficits, abnormally located glutamatergic neurons in layers V-VI of the somatosensory cortex, a 16% increase in activated microglia, and a 15-52% decrease in glutamatergic synapses in layers of the prefrontal and somatosensory cortices. Thus, in utero exposure to CASPR2-antibodies led to permanent behavioral, cellular, and synaptic abnormalities. These findings support a pathogenic role for maternal antibodies in human neurodevelopmental conditions, and CASPR2 as a potential target. Twit Text FOAVip Persistent microglial activation and synaptic loss with behavioral abnormalities in mouse offspring exposed to CASPR2-antibodies in utero ????Acta Neuropathol http://www.kidney.de/pget.php?&tw=1&pmid=28755208 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28755208 #FOAvip English Wikipedia <ref>{{Cite pmid|28755208 }}</ref> Persistent microglial activation and synaptic loss with behavioral abnormalities in mouse offspring exposed to CASPR2-antibodies in utero #MMPMID28755208 Coutinho E ; Menassa DA ; Jacobson L ; West SJ ; Domingos J ; Moloney TC ; Lang B ; Harrison PJ ; Bennett DLH ; Bannerman D ; Vincent A Acta Neuropathol 2017[Oct]; 134 (4 ): 567-583 PMID28755208 show ga Gestational transfer of maternal antibodies against fetal neuronal proteins may be relevant to some neurodevelopmental disorders, but until recently there were no proteins identified. We recently reported a fivefold increase in CASPR2-antibodies in mid-gestation sera from mothers of children with intellectual and motor disabilities. Here, we exposed mice in utero to purified IgG from patients with CASPR2-antibodies (CASPR2-IgGs) or from healthy controls (HC-IgGs). CASPR2-IgG but not HC-IgG bound to fetal brain parenchyma, from which CASPR2-antibodies could be eluted. CASPR2-IgG exposed neonates achieved milestones similarly to HC-IgG exposed controls but, when adult, the CASPR2-IgG exposed progeny showed marked social interaction deficits, abnormally located glutamatergic neurons in layers V-VI of the somatosensory cortex, a 16% increase in activated microglia, and a 15-52% decrease in glutamatergic synapses in layers of the prefrontal and somatosensory cortices. Thus, in utero exposure to CASPR2-antibodies led to permanent behavioral, cellular, and synaptic abnormalities. These findings support a pathogenic role for maternal antibodies in human neurodevelopmental conditions, and CASPR2 as a potential target. |Animals [MESH] |Animals, Outbred Strains [MESH] |Autoantibodies/administration & dosage/*immunology [MESH] |Brain/immunology/pathology [MESH] |Encephalitis/immunology [MESH] |Female [MESH] |Glutamic Acid/metabolism [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Immunoglobulin G/administration & dosage/*metabolism [MESH] |Intracellular Signaling Peptides and Proteins [MESH] |Male [MESH] |Membrane Proteins/deficiency/genetics/*immunology [MESH] |Mice, Knockout [MESH] |Microglia/*immunology/pathology [MESH] |Nerve Tissue Proteins/deficiency/genetics/*immunology [MESH] |Neurons/immunology/pathology [MESH] |Prefrontal Cortex/immunology/pathology [MESH] |Pregnancy [MESH] |Prenatal Exposure Delayed Effects [MESH] |Proteins/*immunology [MESH] |Random Allocation [MESH]Persistent microglial activation and synaptic loss with behavioral abn(epmc).pdf DeepDyve Pubget Overpricing