ArticleTranslational psychiatry2025
Complement C1q is associated with neuroinflammation and mediates the association between amyloid-β and tau pathology in Alzheimer's disease.
Article in Translational psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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
15 citing papers in PubMed.
- From Dysbiosis to Blood-Brain Barrier Disruption: The Metabolite-Mediated Gut-Brain Axis in Alzheimer's Disease.Molecular neurobiology · 2026Review
- Baseline cerebrospinal fluid complement balance is associated with longitudinal memory decline in relation to plasma p‑tau181 levels in mild cognitive impairment.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- The complement system in Alzheimer's disease: evaluating biomarker potential in a complex neuroimmune context.Journal of neuroinflammation · 2026Review
- Neurotransmitter Systems in Alzheimer's Disease.Current issues in molecular biology · 2026Review
- Tau Protein Aggregation Inhibitors-Therapeutic Strategy for Concurrent Tau and Amyloid Aggregation Inhibition.Biomedicines · 2026Review
- Alzheimer's Disease as a Disorder of Neuroimmune Dysregulation.Neurology international · 2026Review
- Complement in brain and eye disease: shared mechanisms, convergent pathologies, and common therapeutic opportunities.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Mapping the Ischemic Continuum: Dynamic Multi-Omic Biomarker and AI for Personalized Stroke Care.International journal of molecular sciences · 2026Review
- The serum C1q-to-CRP ratio performs well for diagnosing periprosthetic joint infection in revision arthroplasty.Frontiers in cellular and infection microbiology · 2026Article
- TREM2 as a central hub of neuroimmune-metabolic crosstalk in central nervous system disorders: from microglial biology to therapeutic targeting.Frontiers in immunology · 2026Review
- Complement and inflammasome crosstalk in chronic inflammation.Frontiers in immunology · 2026Review
- The complement system in Alzheimer's disease: mechanisms, biomarkers, and therapeutic implications.Frontiers in immunology · 2026Review
- Microglial CLEC7A restrains amyloid beta plaque pathology in a mouse model of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Transcriptomic profiling of the middle temporal gyrus reveals differential glial/neuronal dysregulation across Alzheimer's disease and aging.bioRxiv : the preprint server for biology · 2025Article
- Adaptive immune crosstalk and complement dysregulation in the aging retina.Tzu chi medical journalReview
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Complement C1q initiates the classical complement pathway and becomes activated in Alzheimer's disease (AD), contributing to the association between amyloid-β (Aβ) and tau pathologies. However, whether C1q influences AD pathology by modulating glial cell communication is unclear. We included 217 participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database to explore the associations of cerebrospinal fluid (CSF) C1q with soluble triggering receptor expressed on myeloid cells 2 (sTREM2), glial fibrillary acidic protein (GFAP) and AD biomarkers. Additionally, we incorporated data from 535 participants in the Chinese Alzheimer's Biomarker and LifestylE (CABLE) study to explore associations. We employed 10,000 bootstrapped iterations of causal mediation analysis to examine the possible mediating role of sTREM2 or GFAP in the relationship between CSF C1q and AD pathology. We found that CSF rather than serum C1q were positively associated with CSF sTREM2, GFAP, Aβ
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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 Socratic graph.