Genomes and Genes
Amanda J Myers
Affiliation: University of Miami
- AD gene 3-D: moving past single layer genetic information to map novel loci involved in Alzheimer's diseaseAmanda J Myers
Laboratory of Functional Neurogenomics, Department of Psychiatry and Behavioral Sciences, Miller School of Medicine, University of Miami, Miami, FL 33136, USA
J Alzheimers Dis 33:S15-22. 2013..The emphasis will be on taking genomics to the next level by applying additional datasets to truly create maps of a 3-dimensional Alzheimer's genome by including the downstream effects of risk variation...
- The age of the "ome": genome, transcriptome and proteome data set collection and analysisAmanda J Myers
Laboratory of Functional Neurogenomics, University of Miami, Miller School of Medicine, Department of Psychiatry and Behavioral Sciences, Division of Neuroscience, Miami, FL 33136, USA
Brain Res Bull 88:294-301. 2012..This article is part of a Special Issue entitled 'Transcriptome'...
- A survey of genetic human cortical gene expressionAmanda J Myers
Laboratory of Neurogenetics, National Institute on Aging, Porter Neuroscience Building, National Institutes of Health Main Campus, Bethesda, Maryland 20892, USA
Nat Genet 39:1494-9. 2007....
- The MAPT H1c risk haplotype is associated with increased expression of tau and especially of 4 repeat containing transcriptsAmanda J Myers
Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, 35 Convent Drive, Bethesda, MD 20892 3707, USA
Neurobiol Dis 25:561-70. 2007..We discuss these findings both in terms of the problems facing the dissection of the etiologies of complex traits and the pathogenesis of the tauopathies...
- Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's diseaseAdam C Naj
The John P Hussman Institute for Human Genomics, University of Miami, Miami, Florida, USA
Nat Genet 43:436-41. 2011..3 × 10(-8), P(J) = 1.9 × 10(-8)), BIN1 (rs7561528; P(M) = 4.0 × 10(-14), P(J) = 5.2 × 10(-14)) and PICALM (rs561655; P(M) = 7.0 × 10(-11), P(J) = 1.0 × 10(-10)), but not at EXOC3L2, to late-onset Alzheimer's disease susceptibility...
- The structure of the tau haplotype in controls and in progressive supranuclear palsyAlan M Pittman
Reta Lila Weston Institute of Neurological Studies, University College London, UK
Hum Mol Genet 13:1267-74. 2004..We show that the entire, fully extended H1 haplotype is associated with PSP, which implicates several other genes in addition to MAPT, as candidate pathogenic loci...
- A high-density whole-genome association study reveals that APOE is the major susceptibility gene for sporadic late-onset Alzheimer's diseaseKeith D Coon
Neurogenomics Division, Translational Genomics Research Institute, Phoenix, Ariz 85004, USA
J Clin Psychiatry 68:613-8. 2007....
- GAB2 alleles modify Alzheimer's risk in APOE epsilon4 carriersEric M Reiman
Neurogenomics Division, Translational Genomics Research Institute, Phoenix, AZ, 85004, USA
Neuron 54:713-20. 2007..Our findings suggest that GAB2 modifies LOAD risk in APOE epsilon4 carriers and influences Alzheimer's neuropathology...
- THE HUMAN BRAINOME:genome, transcriptome and proteome interaction in human cortexAmanda Myers; Fiscal Year: 2009..This information will help us to define the downstream significance of DNA risk variation in Alzheimer's disease, which might aid in the discovery of novel biomarkers and therapies for this devastating illness. ..
- THE HUMAN BRAINOME:genome, transcriptome and proteome interaction in human cortexAmanda J Myers; Fiscal Year: 2010..This information will help us to define the downstream significance of DNA risk variation in Alzheimer's disease, which might aid in the discovery of novel biomarkers and therapies for this devastating illness. ..