ArticleAmerican journal of human genetics2002
A second locus for very-late-onset Alzheimer disease: a genome scan reveals linkage to 20p and epistasis between 20p and the amyloid precursor protein region.
Article in American journal of human genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 92 citations in OpenAlex.
- Dissecting Complex and Multifactorial Nature of Alzheimer's Disease Pathogenesis: a Clinical, Genomic, and Systems Biology Perspective.Molecular neurobiology · 2016Pooled it
- Alpha-1-antichymotrypsin (ACT or SERPINA3) polymorphism may affect age-at-onset and disease duration of Alzheimer's disease.Neurobiology of aging · 2006Trial
- Genomic variants, genes, and pathways of Alzheimer's disease: An overview.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2017Review
- Cystatin C in aging and in Alzheimer's disease.Ageing research reviews · 2016Review
- The genetic architecture of Alzheimer's disease: beyond APP, PSENs and APOE.Neurobiology of aging · 2012Review
- Cystatin C in Alzheimer's disease.Frontiers in molecular neuroscience · 2012Article
- Protective mechanisms by cystatin C in neurodegenerative diseases.Frontiers in bioscience (Scholar edition) · 2011Review
- Dementia revealed: novel chromosome 6 locus for late-onset Alzheimer disease provides genetic evidence for folate-pathway abnormalities.PLoS genetics · 2010Article
- An ensemble learning approach jointly modeling main and interaction effects in genetic association studies.Genetic epidemiology · 2008Article
- Confronting complexity in late-onset Alzheimer disease: application of two-stage analysis approach addressing heterogeneity and epistasis.Genetic epidemiology · 2008Article
- Age-at-onset linkage analysis in Caribbean Hispanics with familial late-onset Alzheimer's disease.Neurogenetics · 2008Article
- An AICD-based functional screen to identify APP metabolism regulators.Molecular neurodegeneration · 2007Article
- Genetics of Alzheimer's disease: a centennial review.Neurologic clinics · 2007Review
- A genomewide screen for late-onset Alzheimer disease in a genetically isolated Dutch population.American journal of human genetics · 2007Article
- Single cell gene expression profiling in Alzheimer's disease.NeuroRx : the journal of the American Society for Experimental NeuroTherapeutics · 2006Review
- Promoter mutations that increase amyloid precursor-protein expression are associated with Alzheimer disease.American journal of human genetics · 2006Article
- Genome scan on Swedish Alzheimer's disease families.Molecular psychiatry · 2006Article
- Roles of cholesterol and lipids in the etiopathogenesis of Alzheimer's disease.Journal of biomedicine & biotechnology · 2006Article
- The role of cystatin C in cerebral amyloid angiopathy and stroke: cell biology and animal models.Brain pathology (Zurich, Switzerland) · 2006Review
- Fine mapping of 10q and 18q for familial Alzheimer's disease in Caribbean Hispanics.Molecular psychiatry · 2004Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
We used a covariate-based linkage method to reanalyze genome scan data from affected sibships collected by the Alzheimer Disease (AD) Genetics Initiative of the National Institute of Mental Health. As reported in an earlier article, the amyloid-beta precursor protein (APP) region is strongly linked to affected sib pairs of the oldest current age (i.e., age either at last exam or at death) who lack E4 alleles at the apolipoprotein E (ApoE) locus. We now report that a region on 20p shows the same pattern. A model that includes current age and the number of E2 alleles as covariates gives a LOD score of 4.1. The signal on 20p is near the location of the gene coding for cystatin-C, previously shown to be associated with late-onset AD and to codeposit with APP in the brains of patients with AD. Two-locus analysis provides evidence of strong epistasis between 20p and the APP region, limited to the oldest age group and to those lacking ApoE4 alleles. We speculate that high-risk polymorphisms in both regions produce a biological interaction between these two proteins that increases susceptibility to a very-late-onset form of AD.
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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.