ArticleMolecular neuropsychiatry2017
Complement C3 Expression Is Decreased in Autism Spectrum Disorder Subjects and Contributes to Behavioral Deficits in Rodents.
Article in Molecular neuropsychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 70 citations in OpenAlex.
- Peripheral complement proteins in schizophrenia: A systematic review and meta-analysis of serological studies.Schizophrenia research · 2020Pooled it
- Oxytocin and RAGE signaling at the intersection of social neurodevelopment and inflammation.Journal of translational medicine · 2026Review
- Article
- Complement pathway dysregulation and astrocyte alterations in Down syndrome: evidence from postmortem brain tissue and iPSC-derived astrocytes.Acta neuropathologica communications · 2025Article
- Emerging role of complement system in the induction of neuroinflammation in adenylosuccinate lyase deficiency disorder.Brain, behavior, & immunity - health · 2025Review
- The Role of the Complement C3-Hippocampus Pathway in Relation With Mood Symptoms in Offspring of Parents With Bipolar Disorder.Bipolar disorders · 2025Article
- CRISPRi-based screen of autism spectrum disorder risk genes in microglia uncovers roles of ADNP in microglia endocytosis and synaptic pruning.Molecular psychiatry · 2025Article
- Complement system dysfunction in autism spectrum disorder: evidence for altered C1q and C3 levels (complement system dysfunction in ASD).Acta neuropsychiatrica · 2025Article
- Knowing the enemy: strategic targeting of complement to treat Alzheimer disease.Nature reviews. Neurology · 2025Review
- Neuronal CD47 induces behavioral alterations and ameliorates microglial synaptic pruning in wild-type and Alzheimer's mouse models.Cell & bioscience · 2025Article
- Acupuncture enhances fatty acid catabolism and immune modulation in children with autism.Frontiers in psychiatry · 2025Article
- CRISPRi-based screen of Autism Spectrum Disorder risk genes in microglia uncovers roles ofbioRxiv : the preprint server for biology · 2024Article
- Mitochondrial DNA Haplogroup K Is Protective Against Autism Spectrum Disorder Risk in Populations of European Ancestry.Journal of the American Academy of Child and Adolescent Psychiatry · 2024Article
- PolyI:C Maternal Immune Activation on E9.5 Causes the Deregulation of Microglia and the Complement System in Mice, Leading to Decreased Synaptic Spine Density.International journal of molecular sciences · 2024Article
- GEO dataset mining analysis reveals novelFrontiers in molecular biosciences · 2024Article
- Hippocampal Upregulation of Complement Component C3 in Response to Lipopolysaccharide Stimuli in a Model of Fragile-X Syndrome.Current issues in molecular biology · 2023Article
- A Systematic Investigation of Complement and Coagulation-Related Protein in Autism Spectrum Disorder Using Multiple Reaction Monitoring Technology.Neuroscience bulletin · 2023Article
- Roles of complement system in psychiatric disorders.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2023Article
- The NO Answer for Autism Spectrum Disorder.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Autism spectrum disorder (ASD) is a neurodevelopmental disorder with hallmark symptoms including social deficits, communication deficits and repetitive behaviors. Accumulating evidence suggests a potential role of the immune system in the pathophysiology of ASD. The complement system represents one of the major effector mechanisms of the innate immune system, and regulates inflammation, and orchestrates defense against pathogens. However, the role of CNS complement system in ASD is not well understood. In the present study, we found a significant increase in C2, C5, and MASP1, but a decrease in C1q, C3, and C4 mRNA levels in the middle frontal gyrus of ASD subjects compared to controls. Significant decreases in the mRNA levels of 2 key proinflammatory cytokines, IL-17 and IL-23 were observed in ASD subjects. Our study further demonstrated a strong association of complement genes with IL-17 and IL-23, suggesting a possible role of the complement system in immune dysregulation in ASD. We observed significant associations between complement components and abnormality of development scores in subjects with ASD. In rodents, C3 knockdown in the prefrontal cortex induced social interaction deficits and repetitive behavior in mice. Together, these studies suggest a potential role of C3 in the pathophysiology of ASD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.