ArticleBiological psychiatry2013
Effect of complement CR1 on brain amyloid burden during aging and its modification by APOE genotype.
Article in Biological psychiatry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.
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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.
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Who cites it
58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 96 citations in OpenAlex.
- Complement receptor 1 genetic polymorphism contributes to sporadic Alzheimer's disease susceptibility in Caucasians: a meta-analysis.Bioscience reports · 2020Pooled it
- Genetic analysis of quantitative phenotypes in AD and MCI: imaging, cognition and biomarkers.Brain imaging and behavior · 2014Pooled it
- 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
- Microglia Signatures: A Cause or Consequence of Microglia-Related Brain Disorders?International journal of molecular sciences · 2024Review
- Beneficial versus Detrimental Effects of Complement-Microglial Interactions in Alzheimer's Disease.Brain sciences · 2024Review
- The Importance of Complement-Mediated Immune Signaling in Alzheimer's Disease Pathogenesis.International journal of molecular sciences · 2024Review
- Interpretation of Neurodegenerative GWAS Risk Alleles in Microglia and their Interplay with Other Cell Types.Advances in neurobiology · 2024Review
- Recent Trends in Active and Passive Immunotherapies of Alzheimer's Disease.Antibodies (Basel, Switzerland) · 2023Review
- Article
- Brain structure and allelic associations in Alzheimer's disease.CNS neuroscience & therapeutics · 2023Article
- A review of brain imaging biomarker genomics in Alzheimer's disease: implementation and perspectives.Translational neurodegeneration · 2022Review
- Crry silencing alleviates Alzheimer's disease injury by regulating neuroinflammatory cytokines and the complement system.Neural regeneration research · 2022Article
- Neuroinflammatory Signaling in the Pathogenesis of Alzheimer's Disease.Current neuropharmacology · 2022Review
- Spatiotemporal patterns of gliosis and neuroinflammation in presenilin 1/2 conditional double knockout mice.Frontiers in aging neuroscience · 2022Article
- Unified AI framework to uncover deep interrelationships between gene expression and Alzheimer's disease neuropathologies.Nature communications · 2021Article
- NLRP3 and Infections: β-Amyloid in Inflammasome beyond Neurodegeneration.International journal of molecular sciences · 2021Review
- Microglial Responses to Brain Injury and Disease: Functional Diversity and New Opportunities.Translational stroke research · 2021Review
- Microglia and modifiable life factors: Potential contributions to cognitive resilience in aging.Behavioural brain research · 2021Review
- Complement Activation in the Central Nervous System: A Biophysical Model for Immune Dysregulation in the Disease State.Frontiers in molecular neuroscience · 2021Article
- Impacts of CR1 genetic variants on cerebrospinal fluid and neuroimaging biomarkers in alzheimer's disease.BMC medical genetics · 2020Article
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Authors and funding
12 authors at 6 institutions in 1 country.
Funding
Abstract
backgroundThe rs3818361 single nucleotide polymorphism in complement component (3b/4b) receptor-1 (CR1) is associated with increased risk of Alzheimer's disease (AD). Although this novel variant is associated with a small effect size and is unlikely to be useful as a predictor of AD risk, it might provide insights into AD pathogenesis. We examined the association between rs3818361 and brain amyloid deposition in nondemented older individuals.
methodsWe used (11)C-Pittsburgh Compound-B positron emission tomography to quantify brain amyloid burden in 57 nondemented older individuals (mean age 78.5 years) in the neuroimaging substudy of the Baltimore Longitudinal Study of Aging. In a replication study, we analyzed (11)C-Pittsburgh Compound-B positron emission tomography data from 22 cognitively normal older individuals (mean age 77.1 years) in the Alzheimer's Disease Neuroimaging Initiative dataset.
resultsRisk allele carriers of rs3818361 have lower brain amyloid burden relative to noncarriers. There is a strikingly greater variability in brain amyloid deposition in the noncarrier group relative to risk carriers, an effect explained partly by APOE genotype. In noncarriers of the CR1 risk allele, APOE ε4 individuals showed significantly higher brain amyloid burden relative to APOE ε4 noncarriers. We also independently replicate our observation of lower brain amyloid burden in risk allele carriers of rs3818361 in the Alzheimer's Disease Neuroimaging Initiative sample.
conclusionsOur findings suggest complex mechanisms underlying the interaction of CR1, APOE, and brain amyloid pathways in AD. Our results are relevant to treatments targeting brain Aβ in nondemented individuals at risk for AD and suggest that clinical outcomes of such treatments might be influenced by complex gene-gene interactions.
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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.