ArticleAmerican journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics2008
A genomic scan for age at onset of Alzheimer's disease in 437 families from the NIMH Genetic Initiative.
Article in American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Effects of multiple genetic loci on age at onset in late-onset Alzheimer disease: a genome-wide association study.JAMA neurology · 2014Pooled it
- Polygenic inheritance of paclitaxel-induced sensory peripheral neuropathy driven by axon outgrowth gene sets in CALGB 40101 (Alliance).The pharmacogenomics journal · 2014Trial
- Identification of genetic heterogeneity of Alzheimer's disease across age.Neurobiology of aging · 2019Article
- Brain properties predict proximity to symptom onset in sporadic Alzheimer's disease.Brain : a journal of neurology · 2018Article
- Family-based genome scan for age at onset of late-onset Alzheimer's disease in whole exome sequencing data.Genes, brain, and behavior · 2015Article
- Apolipoprotein E, gender, and Alzheimer's disease: an overlooked, but potent and promising interaction.Brain imaging and behavior · 2014Review
- Alzheimer's disease risk genes and the age-at-onset phenotype.Neurobiology of aging · 2013Article
- Genome scan in familial late-onset Alzheimer's disease: a locus on chromosome 6 contributes to age-at-onset.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2013Article
- A PIN1 polymorphism that prevents its suppression by AP4 associates with delayed onset of Alzheimer's disease.Neurobiology of aging · 2012Article
- Genome scan of age-at-onset in the NIMH Alzheimer disease sample uncovers multiple loci, along with evidence of both genetic and sample heterogeneity.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2011Article
- Evidence for three loci modifying age-at-onset of Alzheimer's disease in early-onset PSEN2 families.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2010Article
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Authors and funding
7 authors.
Funding
Abstract
We performed linkage analysis for age at onset (AAO) in the total Alzheimer's disease (AD) NIMH sample (N = 437 families). Families were subset as late-onset (320 families, AAO > or = 65) and early/mixed (117 families, at least 1 member with 50 < AAO < 65). Treating AAO as a censored trait, we obtained the gender and APOE adjusted residuals in a parametric survival model and analyzed the residuals as the quantitative trait (QT) in variance-component linkage analysis. For comparison, AAO-age at exam (AAE) was analyzed as the QT adjusting for affection status, gender, and APOE. Heritabilities for residual and AAO-AAE outcomes were 66.3% and 74.0%, respectively for the total sample, 56.0% and 57.0% in the late-onset sample, and 33.0% for both models in the early/mixed sample. The residual model yielded the largest peaks on chromosome 1 with LOD = 2.0 at 190 cM in the total set, LOD = 1.7 at 116 cM on chromosome 3 in the early/mixed subset, and LOD = 1.4 at 71 and 86 cM, respectively, on chromosome 6 in the late-onset subset. For the AAO-AAE outcome model the largest peaks were identified on chromosome 1 at 137 cM (LOD = 2.8) and chromosome 6 at 69 cM (LOD = 2.3) and 86 cM (LOD = 2.2) all in the late-onset subset. Additional peaks with LOD > or = 1 were identified on chromosomes 1, 2, 3, 6, 8, 9, 10, and 12 for the total sample and each subset. Results replicate previous findings, but identify additional suggestive peaks indicating the genetics of AAO in AD is complex with many chromosomal regions potentially containing modifying genes.
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