ReviewFrontiers in immunology2023
C1q and central nervous system disorders.
Review in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
34 citing papers in PubMed, 43 citations in OpenAlex.
- The neuroimmune network in Alzheimer's and Parkinson's diseases: from mechanistic insights to biomarker-guided immunotherapies and clinical translation.Inflammopharmacology · 2026Review
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- Role Shift of Glial Cells from Physiology to Pathology in Alzheimer's Disease: The Regulatory Impact of Exercise.Neuroscience bulletin · 2026Review
- An Open-Label Phase 1b Study of the Safety, Pharmacokinetics, Pharmacodynamics, and Clinical Activity of ANX005 in Patients with Huntington's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Downregulation of neuronal DRD2 drives microglia synaptic pruning and results in cognitive deficits by promoting CCL2 release in a rat model of chronic migraine.The journal of headache and pain · 2026Article
- Reframing brain aging: neuroinflammation as an interconnected network process.Frontiers in aging · 2026Review
- Splenic PD-L1Research (Washington, D.C.) · 2026Article
- Anti-Complementary Constituents From Artemisia vestita Alleviate H1N1-Induced Acute Lung Injury.Chemistry & biodiversity · 2026Article
- Phosphoproteomics uncovers a neuroimmune perspective on trigeminal neuralgia: sexually dimorphic regulatory networks linking calcium channels to the complement cascade.Frontiers in immunology · 2026Article
- C1q limits cystoid edema by maintaining basal β-catenin-dependent signaling and blood-retina barrier function.JCI insight · 2025Article
- Neuroprotective Effects of Ginsenoside Rg3 in Depressed Mice via Inhibition of the C1q Complement Pathway.CNS neuroscience & therapeutics · 2025Article
- Review
- Complement C1q is associated with neuroinflammation and mediates the association between amyloid-β and tau pathology in Alzheimer's disease.Translational psychiatry · 2025Article
- Neuroinflammation: Mechanisms, Dual Roles, and Therapeutic Strategies in Neurological Disorders.Current issues in molecular biology · 2025Review
- Underestimated pyridoxine consumption and neurotoxicity: a novel manifestation with rheumatologic relevance - a case-based review.Rheumatology international · 2025Review
- The E3 ligase c-Cbl modulates microglial phenotypes and contributes to Parkinson's disease pathology.Cell death discovery · 2025Article
- Upregulation of C1QC as a Mediator of Blood-Brain Barrier Damage in Type 2 Diabetes Mellitus.Molecular neurobiology · 2025Article
- Delta-opioid receptor signaling alleviates neuropathology and cognitive impairment in the mouse model of Alzheimer's disease by regulating microglia homeostasis and inhibiting HMGB1 pathway.Alzheimer's research & therapy · 2025Article
- The dual nature of neuroinflammation in networked brain.Frontiers in immunology · 2025Review
- Neuroinflammatory Proteins in Huntington's Disease: Insights into Mechanisms, Diagnosis, and Therapeutic Implications.International journal of molecular sciences · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C1q is a crucial component of the complement system, which is activated through the classical pathway to perform non-specific immune functions, serving as the first line of defense against pathogens. C1q can also bind to specific receptors to carry out immune and other functions, playing a vital role in maintaining immune homeostasis and normal physiological functions. In the developing central nervous system (CNS), C1q functions in synapse formation and pruning, serving as a key player in the development and homeostasis of neuronal networks in the CNS. C1q has a close relationship with microglia and astrocytes, and under their influence, C1q may contribute to the development of CNS disorders. Furthermore, C1q can also have independent effects on neurological disorders, producing either beneficial or detrimental outcomes. Most of the evidence for these functions comes from animal models, with some also from human specimen studies. C1q is now emerging as a promising target for the treatment of a variety of diseases, and clinical trials are already underway for CNS disorders. This article highlights the role of C1q in CNS diseases, offering new directions for the diagnosis and treatment of these conditions.
Indexed as
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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.