ArticleJAMA neurology2013
Genetic susceptibility for Alzheimer disease neuritic plaque pathology.
Article in JAMA neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 8 of them syntheses that pooled it.
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Who cites it
103 citing papers in PubMed, 8 syntheses or guidelines pooled it.
- Systematic review and meta-analysis of the association betweenFrontiers in aging neuroscience · 2024Pooled it
- Interaction Analysis Reveals Complex Genetic Associations with Alzheimer's Disease in theGenes · 2023Pooled it
- Complement receptor 1 genetic polymorphism contributes to sporadic Alzheimer's disease susceptibility in Caucasians: a meta-analysis.Bioscience reports · 2020Pooled it
- A Common DIO2 Polymorphism and Alzheimer Disease Dementia in African and European Americans.The Journal of clinical endocrinology and metabolism · 2018Pooled it
- Updated Meta-Analysis of BIN1, CR1, MS4A6A, CLU, and ABCA7 Variants in Alzheimer's Disease.Journal of molecular neuroscience : MN · 2018Pooled it
- Associations Between Genetic Variants in 19p13 and 19q13 Regions and Susceptibility to Alzheimer Disease: A Meta-Analysis.Medical science monitor : international medical journal of experimental and clinical research · 2016Pooled it
- Analyzing 54,936 Samples Supports the Association Between CD2AP rs9349407 Polymorphism and Alzheimer's Disease Susceptibility.Molecular neurobiology · 2015Pooled it
- Genome-wide association meta-analysis of neuropathologic features of Alzheimer's disease and related dementias.PLoS genetics · 2014Pooled it
- Resilience to cognitive impairment in the oldest-old: design of the EMIF-AD 90+ study.BMC geriatrics · 2018Trial
- A new era of genome-wide association studies in the field of Alzheimer's disease and overlapping co-pathologies: lessons learned from a neuropathology-centered approach.Acta neuropathologica · 2026Review
- Tau seeds induce neurofibrillary tangle formation across brain regions via individual-specific connectivity.Neuron · 2026Article
- Molecular signatures of resilience to Alzheimer's disease in neocortical layer 4 neurons.Nature communications · 2026Article
- APOE, ABCA7, and RASGEF1C are associated with earlier onset of amyloid deposition from more than 4000 harmonized positron emission tomography images.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- CD2AP at the junction of nephropathy and Alzheimer's disease.Molecular neurodegeneration · 2025Review
- Neuronal ABCA7 deficiency aggravates mitochondrial dysfunction and neurodegeneration in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The promise of gene therapy in common types of dementia.BioImpacts : BI · 2025Review
- The Alzheimer's Disease Risk Gene CD2AP Functions in Dendritic Spines by Remodeling F-Actin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Integration across biophysical scales identifies molecular and cellular correlates of person-to-person variability in human brain connectivity.Nature neuroscience · 2024Article
- Integrating amyloid and tau imaging with proteomics and genomics in Alzheimer's disease.Cell reports. Medicine · 2024Review
- Proteins linking APOE ɛ4 with Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
43 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
17 authors.
Funding
Abstract
importanceWhile numerous genetic susceptibility loci have been identified for clinical Alzheimer disease (AD), it is important to establish whether these variants are risk factors for the underlying disease pathology, including neuritic plaques.
objectivesTo investigate whether AD susceptibility loci from genome-wide association studies affect neuritic plaque pathology and to additionally identify novel risk loci for this trait. DESIGN, SETTING, AND
participantsCandidate analysis of single-nucleotide polymorphisms and genome-wide association study in a joint clinicopathologic cohort, including 725 deceased subjects from the Religious Orders Study and the Rush Memory and Aging Project (2 prospective, community-based studies), followed by targeted validation in an independent neuroimaging cohort, including 114 subjects from multiple clinical and research centers. MAIN OUTCOMES AND MEASURES: A quantitative measure of neuritic plaque pathologic burden, based on assessments of silver-stained tissue averaged from multiple brain regions. Validation based on β-amyloid load by immunocytochemistry, and replication with fibrillar β-amyloid positron emission tomographic imaging with Pittsburgh Compound B or florbetapir.
resultsBesides the previously reported APOE and CR1 loci, we found that the ABCA7 (rs3764650; P = .02) and CD2AP (rs9349407; P = .03) AD susceptibility loci are associated with neuritic plaque burden. In addition, among the top results of our genome-wide association study, we discovered a novel variant near the amyloid precursor protein gene (APP, rs2829887) that is associated with neuritic plaques (P = 3.3 × 10-6). This polymorphism was associated with postmortem β-amyloid load as well as fibrillar β-amyloid in 2 independent cohorts of adults with normal cognition. CONCLUSIONS AND RELEVANCE: These findings enhance understanding of AD risk factors by relating validated susceptibility alleles to increased neuritic plaque pathology and implicate common genetic variation at the APP locus in the earliest, presymptomatic stages of AD.
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