ArticleMolecular psychiatry2012
Alzheimer risk associated with a copy number variation in the complement receptor 1 increasing C3b/C4b binding sites.
Article in Molecular psychiatry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 9 of them syntheses that pooled it.
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Who cites it
140 citing papers in PubMed, 9 syntheses or guidelines pooled it, 231 citations in OpenAlex.
- Guidelines for bioinformatics of single-cell sequencing data analysis in Alzheimer's disease: review, recommendation, implementation and application.Molecular neurodegeneration · 2022Pooled it
- Microglial Phagocytosis: A Disease-Associated Process Emerging from Alzheimer's Disease Genetics.Trends in neurosciences · 2020Pooled it
- Pooled it
- Complement receptor 1 genetic polymorphism contributes to sporadic Alzheimer's disease susceptibility in Caucasians: a meta-analysis.Bioscience reports · 2020Pooled it
- Genetic meta-analysis of diagnosed Alzheimer's disease identifies new risk loci and implicates Aβ, tau, immunity and lipid processing.Nature genetics · 2019Pooled it
- Copy Number Variants in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2017Pooled it
- Genetic analysis of quantitative phenotypes in AD and MCI: imaging, cognition and biomarkers.Brain imaging and behavior · 2014Pooled it
- Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease.Nature genetics · 2013Pooled it
- Pooled it
- Complement component C4 regulates amyloid pathology and glial reactivity in mouse model of Alzheimer's Disease.bioRxiv : the preprint server for biology · 2026Article
- Advancements in the Study of Missense Mutations in ABCA7 in Alzheimer's Disease.Journal of molecular neuroscience : MN · 2026Review
- Age-related macular degeneration and cerebral amyloid angiopathy have similar pathologies from cholesterol-APOE-amyloid-β-complement mediated inflammation.Progress in retinal and eye research · 2026Review
- Dark and camouflaged genomic regions remain challenging in CHM13.Scientific reports · 2026Article
- Alzheimer's disease: genetic background in the era of next-generation sequencing technologies.Brain communications · 2026Review
- Inflammatory mechanisms underlying early Alzheimer's disease pathology: evidence from the aging rhesus macaque brain.Frontiers in cellular neuroscience · 2026Review
- The complement cascade in Alzheimer's disease: modern implications of an ancient immune protagonist.Molecular neurodegeneration · 2025Review
- fSuSiE enables fine-mapping of QTLs from genome-scale molecular profiles.bioRxiv : the preprint server for biology · 2025Article
- Integrated genetic analysis of Alzheimer's disease and stroke subtypes: insights from LDSC, PLACO, and MR studies.BMC neurology · 2025Article
- The Alzheimer's disease-associated complement receptor 1 variant confers risk by impacting glial phagocytosis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Phage-Microbiota Crosstalk: Implications for Central Nervous System Disorders.International journal of molecular sciences · 2025Review
80 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Two multicentre genome-wide association (GWA) studies provided substantial evidence, implicating the complement receptor 1 gene (CR1) in Alzheimer disease (AD) genetic etiology. CR1 encodes a large transmembrane receptor with a crucial role in the immune complement cascade. We performed a genetic follow-up of the GWA CR1 association in a Flanders-Belgian cohort (n=1883), and investigated the effect of single-nucleotide polymorphisms (SNPs) located in the CR1 locus on AD risk and cerebrospinal fluid (CSF) biomarker levels. We obtained significant association (P(adj)<0.03; odds ratio (OR)=1.24 (95% confidence interval (CI): 1.02-1.51)) for one CR1 risk haplotype, and haplotype association was strongest in individuals carrying apolipoprotein E (APOE) ɛ4 alleles (P(adj)<0.006; OR=1.50 (95% CI: 1.08-2.09)). Also, four SNPs correlated with increased CSF amyloid Aβ₁₋₄₂ levels, suggesting a role for the CR1 protein in Aβ metabolism. Moreover, we quantified a low-copy repeat (LCR)-associated copy number variation (CNV) in CR1, producing different CR1 isoforms, CR1-F and CR1-S, and obtained significant association in carriers of CR1-S. We replicated the CR1 CNV association finding in a French cohort (n=2003) and calculated in the combined cohorts, an OR of 1.32; 95% CI: 1.10-1.59 (P=0.0025). Our data showed that the common AD risk association may well be explained by the presence of CR1-S increasing the number of C3b/C4b and cofactor activity sites and AD risk with 30% in CR1-S carriers. How precisely the different functional role of CR1-S in the immune complement cascade contributes to AD pathogenesis will need additional functional studies.
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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.