ReviewMediators of inflammation2018
Contribution of Neurons and Glial Cells to Complement-Mediated Synapse Removal during Development, Aging and in Alzheimer's Disease.
Review in Mediators of inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 51 papers, 2 of them syntheses that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
51 citing papers in PubMed, 2 syntheses or guidelines pooled it, 85 citations in OpenAlex.
- The Role of Astrocytes in Synapse Loss in Alzheimer's Disease: A Systematic Review.Frontiers in cellular neuroscience · 2022Pooled it
- Complement receptor 1 genetic polymorphism contributes to sporadic Alzheimer's disease susceptibility in Caucasians: a meta-analysis.Bioscience reports · 2020Pooled it
- Short-chain fatty acid-producing commensals: Key modulators of AD neuroinflammation via the microbiota-gut-brain axis.Current research in microbial sciences · 2026Review
- miR-214-3p and NCKAP1: A microglial functional dimension of Alzheimer's progression.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- C1qa muscularis macrophages maintain enteric synaptic homeostasis to regulate gastrointestinal motility.bioRxiv : the preprint server for biology · 2026Article
- Diminished activity-dependent neuroprotective protein (ADNP) contributes to complement gene elevation in Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2026Article
- The Immuno-Glial Connectome in Alzheimer's Disease: Integrating Central and Peripheral Inflammatory Networks.Cellular and molecular neurobiology · 2026Review
- C3 lowering in adult APP KI mice rescues synapses and spares cognitive decline.Molecular neurodegeneration advances · 2026Article
- Redox modulation of the complement cascade contributes to synapse loss in Alzheimer's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- Age-Related Complement C3 Drives Memory Impairments and Associated Neuropathologies in a Mouse Model.Aging cell · 2025Article
- Cross-Species Modeling Identifies Gene Signatures in Type 2 Diabetes Mouse Models Predictive of Inflammatory and Estrogen Signaling Pathways Associated with Alzheimer's Disease Outcomes in Humans.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2025Article
- SVHRSP Alleviates Age-Related Cognitive Deficiency by Reducing Oxidative Stress and Neuroinflammation.Antioxidants (Basel, Switzerland) · 2024Article
- Single cell transcriptome analysis of the THY-Tau22 mouse model of Alzheimer's disease reveals sex-dependent dysregulations.Cell death discovery · 2024Article
- Complement C3 From Astrocytes Plays Significant Roles in Sustained Activation of Microglia and Cognitive Dysfunctions Triggered by Systemic Inflammation After Laparotomy in Adult Male Mice.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Article
- α-Synuclein oligomers potentiate neuroinflammatory NF-κB activity and induce CaTranslational neurodegeneration · 2024Article
- As a Potential Therapeutic Target, C1q Induces Synapse Loss Via Inflammasome-activating Apoptotic and Mitochondria Impairment Mechanisms in Alzheimer's Disease.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023Review
- Dietary fatty acids differentially impact phagocytosis, inflammatory gene expression, and mitochondrial respiration in microglial and neuronal cell models.Frontiers in cellular neuroscience · 2023Article
- The gut microbiota in neurodegenerative diseases: revisiting possible therapeutic targets for cannabidiol.Heliyon · 2022Review
- FTH1- and SAT1-Induced Astrocytic Ferroptosis Is Involved in Alzheimer's Disease: Evidence from Single-Cell Transcriptomic Analysis.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Elevated CSF and plasma complement proteins in genetic frontotemporal dementia: results from the GENFI study.Journal of neuroinflammation · 2022Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synapse loss is an early manifestation of pathology in Alzheimer's disease (AD) and is currently the best correlate to cognitive decline. Microglial cells are involved in synapse pruning during development via the complement pathway. Moreover, recent evidence points towards a key role played by glial cells in synapse loss during AD. However, further contribution of glial cells and the role of neurons to synapse pathology in AD remain not well understood. This review is aimed at comprehensively reporting the source and/or cellular localization in the CNS-in microglia, astrocytes, or neurons-of the triggering components (C1q, C3) of the classical complement pathway involved in synapse pruning in development, adulthood, and AD.
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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.