ReviewWIREs mechanisms of disease2022
Complement and microglia dependent synapse elimination in brain development.
Review in WIREs mechanisms of disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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.
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
53 citing papers in PubMed, 57 citations in OpenAlex.
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- Natural Products and Neuroregeneration: Rethinking Discovery Beyond Bioavailability Through Pseudo-Natural Product Design.Biomedicines · 2026Review
- Review
- The Oral-Brain Axis: A Unified Framework Linking Trigeminal Sensorimotor Dysfunction, Chronic Stress, Neuroinflammation, and Neurodegeneration.International journal of molecular sciences · 2026Review
- Targeting the Complement-Microglia Axis for Neuroprotection in Pediatric Epilepsy.Biomedicines · 2026Review
- Positive selection on brain cis-regulatory elements in the human lineage drives changes in gene expression and susceptibility to neuropsychiatric disorders.HGG advances · 2026Article
- Dissecting PANoptosis in the Nervous System: A Unified Cell-Death Mechanism Driving Neuroimmune Activation and Chronic Neuroinflammation.Molecular neurobiology · 2026Review
- C1qa muscularis macrophages maintain enteric synaptic homeostasis to regulate gastrointestinal motility.bioRxiv : the preprint server for biology · 2026Article
- Microglia-Mediated Dysfunction of PKCγ Interneurons Underlies the Mechanical Hypersensitivity in Autism.Molecular neurobiology · 2026Article
- Glaucoma and Autoimmunity: Immunopathogenic Mechanisms and Emerging Immunomodulatory Therapies.Biomedicines · 2026Review
- Neurovascular and synaptic milieu of brain-resident cells in cognitive dysfunction of myalgic encephalomyelitis/chronic fatigue syndrome.Journal of translational medicine · 2026Review
- The aging gut-glia-immune axis in alzheimer's disease: microbiome-derived mediators of neuroinflammation and therapeutic innovation.GeroScience · 2026Review
- Alzheimer's Disease as a Disorder of Neuroimmune Dysregulation.Neurology international · 2026Review
- C1q neutralization during epileptogenesis attenuates complement-mediated synaptic elimination and epileptiform activity.Epilepsia · 2026Article
- The glia-immune network: Astrocytes and oligodendrocytes as microglial co-ordinators in health and disease.The Journal of physiology · 2026Review
- Oxytocin Modulates Microglial IL-17-Linked Inflammatory Pathways Through the IL-6/COX-2.Life (Basel, Switzerland) · 2026Article
- Glial Cell Dynamics in Neuroinflammation: Mechanisms, Interactions, and Therapeutic Implications.Biomedicines · 2026Review
- Peripheral complement C3 and C4 are associated with clinical features of schizophrenia.Frontiers in psychiatry · 2026Article
- Targeting Microglial Phagocytosis for Alzheimer's Disease Management: Natural, Pharmacological, Nanoparticle, and Gene Therapy Approaches.CNS & neurological disorders drug targets · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Synapse elimination, also known as synaptic pruning, is a critical step in the maturation of neural circuits during brain development. Mounting evidence indicates that the complement cascade of the innate immune system plays an important role in synapse elimination. Studies indicate that excess synapses during development are opsonized by complement proteins and subsequently phagocytosed by microglia which expresses complement receptors. The process is regulated by diverse molecular signals, including complement inhibitors that affect the activation of complement, as well as signals that affect microglial recruitment and activation. These signals may promote or inhibit the removal of specific sets of synapses during development. The complement-microglia system has also been implicated in the pathogenesis of several developmental brain disorders, suggesting that the dysregulation of mechanisms of synapse pruning may underlie the specific circuitry defects in these diseases. Here, we review the latest evidence on the molecular and cellular mechanisms of complement-dependent and microglia-dependent synapse elimination during brain development, and highlight the potential of this system as a therapeutic target for developmental brain disorders. This article is categorized under: Neurological Diseases > Molecular and Cellular Physiology Neurological Diseases > Stem Cells and Development Immune System Diseases > Molecular and Cellular Physiology.
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What OpenQuestion holds
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.