ReviewAging and disease2019
Emerging Roles of Complement Protein C1q in Neurodegeneration.
Review in Aging and disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 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
50 citing papers in PubMed, 76 citations in OpenAlex.
- A human pluripotent stem cell triculture platform to elucidate microglial regulation of retinal ganglion cells in neuroinflammation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Targeting Complement Component 1q Ameliorates Diabetic Endothelial Inflammation Via Orphan Nuclear Receptor 4a1-Dependent Suppression of Nuclear Factor κB Signaling.Journal of the American Heart Association · 2026Article
- C3 lowering in adult APP KI mice rescues synapses and spares cognitive decline.Molecular neurodegeneration advances · 2026Article
- Emerging pathological mechanisms of Alzheimer's disease pathogenesis: from neuroimmune interactions to intercellular communication.Frontiers in aging neuroscience · 2026Review
- Neurovascular Dysfunction and Glymphatic Impairment: An Unexplored Therapeutic Frontier in Neurodegeneration.International journal of molecular sciences · 2025Review
- Review
- Exploring immunotherapeutic strategies for neurodegenerative diseases: a focus on Huntington's disease and Prion diseases.Acta pharmacologica Sinica · 2025Review
- Complement system dysfunction in autism spectrum disorder: evidence for altered C1q and C3 levels (complement system dysfunction in ASD).Acta neuropsychiatrica · 2025Article
- Xixin Decoction May Treat Vascular Dementia by Modulating the NPTX2/C1q/C3 Complement Pathway.Chemistry & biodiversity · 2025Article
- Astrocytic Hevin/SPARCL-1 Regulates Cognitive Decline in Pathological and Normal Brain Aging.Aging cell · 2025Article
- SIRT1-based therapy targets a gene program involved in mitochondrial turnover in a model of retinal neurodegeneration.Scientific reports · 2025Article
- A Pilot Proteomic Analysis of Huntington's Disease by Functional Capacity.Brain sciences · 2025Article
- The interaction of tPA with NMDAR1 drives neuroinflammation and neurodegeneration in α-synuclein-mediated neurotoxicity.Journal of neuroinflammation · 2025Article
- Generation of decellularized human brain tissue for investigating cell-matrix interactions: a proof-of-concept study.Frontiers in bioengineering and biotechnology · 2025Article
- Distinct neuroprotective and anti-inflammatory effects of Kampo formulas ninjinyoeito and juzentaihoto in depression-like SAMP8 mice.Frontiers in pharmacology · 2025Article
- Revolutionizing Neuroimmunology: Unraveling Immune Dynamics and Therapeutic Innovations in CNS Disorders.International journal of molecular sciences · 2024Review
- Nuclear alpha-synuclein accelerates cell senescence and neurodegeneration.Immunity & ageing : I & A · 2024Article
- Brain-derived neurotrophic factor from microglia regulates neuronal development in the medial prefrontal cortex and its associated social behavior.Molecular psychiatry · 2024Article
- New Insights into Oxidative Stress and Inflammatory Response in Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Complement C1q essential for aeroallergen sensitization via CSF1RThe Journal of allergy and clinical immunology · 2023Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The innate immune system is an ancient and primary component system that rapidly reacts to defend the body against external pathogens. C1 is the initial responder of classical pathway of the innate immune system. C1 is comprised of C1q, C1r, and C1s. Among them, C1q is known to interact with diverse ligands, which can perform various functions in physiological and pathophysiological conditions. Because C1q participates in the clearance of pathogens, its interaction with novel receptors is expected to facilitate apoptosis induction, which could prevent the onset or progression of neurodegenerative diseases and could delay the aging process. Because senescence-associated secreting phenotype determinants are generally inflammatory cytokines or immune factors to activate immune cells. In the central nervous system, C1q has diverse neuroprotective roles against pathogens and inflammation. Most of neurodegenerative diseases show region specific pathology feature in the brain. It has been suggested the evidences that the active site and amount of C1q may be disease specific. This review considers currently the emerging and under-recognized roles of C1q in neurodegeneration and highlights the need for further research to clarify these roles. Future studies on the roles of C1q in regulating disease progression should consider these aspects, including the age-dependent onset time of each neurodegenerative disease progression.
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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.