ArticleActa neuropathologica2017
Persistent microglial activation and synaptic loss with behavioral abnormalities in mouse offspring exposed to CASPR2-antibodies in utero.
Article in Acta neuropathologica, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 57 citations in OpenAlex.
- Captopril restores microglial homeostasis and reverses ASD-like phenotype in a model of ASD induced by exposure in utero to anti-caspr2 IgG.Molecular psychiatry · 2026Article
- CASPR2 Autoimmune Antibodies Induce Neuronal Hyperactivity in Human Brain Organoids.Journal of neurochemistry · 2026Article
- Heterogeneity of anti-Caspr2 antibodies: specificity and pathogenicity.Translational psychiatry · 2025Article
- Clinical data and reporting quality in NMDAR-antibody encephalitis and pregnancy: a systematic review.BMJ neurology open · 2025Article
- Transient CSF1R inhibition ameliorates behavioral deficits in Cntnap2 knockout and valproic acid-exposed mouse models of autism.Journal of neuroinflammation · 2024Article
- Exploring causal mechanisms of psychosis risk.Neuroscience and biobehavioral reviews · 2024Review
- Maternal Influenza and Offspring Neurodevelopment.Current issues in molecular biology · 2024Review
- Impaired functional connectivity of the hippocampus in translational murine models of NMDA-receptor antibody associated neuropsychiatric pathology.Molecular psychiatry · 2024Article
- Noteworthy perspectives on microglia in neuropsychiatric disorders.Journal of neuroinflammation · 2023Review
- Maternal brain reactive antibodies profile in autism spectrum disorder: an update.Translational psychiatry · 2023Review
- Investigating behavioral phenotypes related to autism spectrum disorder in a gene-environment interaction model ofFrontiers in neuroscience · 2023Article
- The spatiotemporal dynamics of microglia across the human lifespan.Developmental cell · 2022Article
- Maternal autoantibody profiles as biomarkers for ASD and ASD with co-occurring intellectual disability.Molecular psychiatry · 2022Article
- Autoantibodies in neurological disease.Nature reviews. Immunology · 2021Review
- Inhibition of Maternal-to-Fetal Transfer of IgG Antibodies by FcRn Blockade in a Mouse Model of Arthrogryposis Multiplex Congenita.Neurology(R) neuroimmunology & neuroinflammation · 2021Article
- Autoantibody-associated psychiatric syndromes in children: link to adult psychiatry.Journal of neural transmission (Vienna, Austria : 1996) · 2021Review
- Autism Spectrum Disorders: Multiple Routes to, and Multiple Consequences of, Abnormal Synaptic Function and Connectivity.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2021Review
- Autoimmune Epilepsy - Novel Multidisciplinary Analysis, Discoveries and Insights.Frontiers in immunology · 2021Review
- Histamine, Neuroinflammation and Neurodevelopment: A Review.Frontiers in neuroscience · 2021Review
- In utero exposure to endogenous maternal polyclonal anti-Caspr2 antibody leads to behavioral abnormalities resembling autism spectrum disorder in male mice.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
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.
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Registered trials
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