ArticleScience (New York, N.Y.)2021
Complement factor C1q mediates sleep spindle loss and epileptic spikes after mild brain injury.
Article in Science (New York, N.Y.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers, 1 of them a synthesis that pooled it.
What it found
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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
70 citing papers in PubMed, 1 synthesis or guideline pooled it.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- Effects of high-definition transcranial direct current stimulation for the treatment of chronic insomnia: a randomized, double-blind, controlled trial.Scientific reports · 2025Trial
- Noninvasive ultrashort wave neuromodulation enhances glymphatic clearance to alleviate traumatic brain edema and Alzheimer's pathology.Science advances · 2026Article
- Mild and repetitive mild traumatic brain injury: Changes in microglial cells and synapses.Neural regeneration research · 2026Article
- C1QB-Mediated Immunopathology in a Murine Malaria Model: A Multi-Omics Validation for Diagnostic and Therapeutic Targeting.International journal of molecular sciences · 2026Article
- FcγR- and CD9-dependent synapse-engulfing microglia in the thalamus drive cognitive impairment following cortical brain damage in mice.Nature communications · 2026Article
- Article
- Microglia and neuroinflammation: function, heterogeneity, and crosstalk.Cellular & molecular immunology · 2026Review
- Associations of complement proteins and immunoglobulins with cognitive impairment in type 2 diabetes mellitus: a cross-sectional study.BMC endocrine disorders · 2026Article
- Complement in Traumatic Brain Injury: Linking Acute Injury to Chronic Neurodegeneration.European journal of immunology · 2026Review
- USP4 modulates ZBP1 ubiquitination to regulate microglial PANoptosis and functional outcomes following traumatic brain injury.Cell death and differentiation · 2026Article
- Targeting microglial C1q alleviates blood-brain barrier disruption in the thalamus after cortical infarction.Journal of neuroinflammation · 2026Article
- Comparative analysis of nuclei isolation methods for brain single-nucleus RNA sequencing.Cell reports methods · 2026Article
- Genome-wide consensus transcriptional signatures identify synaptic pruning linking Alzheimer's disease and epilepsy.Molecular psychiatry · 2026Article
- Phagocytosis and neuroinflammation: orchestrating central nervous system homeostasis, repair, and the resolution of inflammation.Trends in neurosciences · 2026Review
- Secondary thalamic neuroinflammation associates with disturbed corticothalamic connectivity in a model of severe traumatic brain injury in male rats-a longitudinal study.Cerebral cortex (New York, N.Y. : 1991) · 2026Article
- Artificial intelligence for automated detection of interictal epileptiform discharges: methodological progress, clinical evaluation, and neurodevelopmental context.Frontiers in cell and developmental biology · 2026Review
- Microglial pathological synaptic pruning in epilepsy: pathophysiology and therapeutic potential.Frontiers in immunology · 2026Review
- C1q drives neural stem cell quiescence by regulating cell cycle and metabolism through BAI1.Nature communications · 2025Article
- Stage-specific TRIM10 expression regulates erythroid maturation.EMBO reports · 2025Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
Abstract
Although traumatic brain injury (TBI) acutely disrupts the cortex, most TBI-related disabilities reflect secondary injuries that accrue over time. The thalamus is a likely site of secondary damage because of its reciprocal connections with the cortex. Using a mouse model of mild TBI (mTBI), we found a chronic increase in C1q expression specifically in the corticothalamic system. Increased C1q expression colocalized with neuron loss and chronic inflammation and correlated with disruption in sleep spindles and emergence of epileptic activities. Blocking C1q counteracted these outcomes, suggesting that C1q is a disease modifier in mTBI. Single-nucleus RNA sequencing demonstrated that microglia are a source of thalamic C1q. The corticothalamic circuit could thus be a new target for treating TBI-related disabilities.
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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.