2023 - Research.com Genetics in United States Leader Award
2009 - Fellow of the American Association for the Advancement of Science (AAAS)
Jonathan L. Haines spends much of his time researching Genetics, Genome-wide association study, Single-nucleotide polymorphism, Alzheimer's disease and Autism. His Genetics study focuses mostly on Locus, Haplotype, Genetic association, Allele and Genetic linkage. His biological study spans a wide range of topics, including Odds ratio, Polymorphism, Genomics, PICALM and Disease.
He combines subjects such as Cancer, Apolipoprotein E, Human genome and Bioinformatics with his study of Single-nucleotide polymorphism. His Alzheimer's disease study integrates concerns from other disciplines, such as Progressive supranuclear palsy, SORL1, Case-control study, Dementia and Age of onset. His research in Autism intersects with topics in Human genetics and Copy-number variation.
His scientific interests lie mostly in Genetics, Disease, Genome-wide association study, Single-nucleotide polymorphism and Alzheimer's disease. His study in Genetics focuses on Locus, Gene, Genetic association, Genetic linkage and Allele. His study in Disease focuses on Late onset in particular.
His Genome-wide association study study combines topics in areas such as Odds ratio, Glaucoma, Bioinformatics and Genomics. His Single-nucleotide polymorphism research focuses on subjects like Internal medicine, which are linked to Macular degeneration. His research on Alzheimer's disease often connects related topics like Apolipoprotein E.
Jonathan L. Haines focuses on Genetics, Disease, Alzheimer's disease, Genome-wide association study and Gene. His works in Genome, Allele, Single-nucleotide polymorphism, Genetic association and Whole genome sequencing are all subjects of inquiry into Genetics. In his study, which falls under the umbrella issue of Genetic association, Genotype is strongly linked to Odds ratio.
His Disease research is multidisciplinary, incorporating perspectives in Meta-analysis, Genetic variants and Risk factor. Within one scientific family, Jonathan L. Haines focuses on topics pertaining to Epidemiology under Alzheimer's disease, and may sometimes address concerns connected to Public health. His Genome-wide association study research incorporates themes from Missense mutation, Intraocular pressure, Linkage disequilibrium, Pedigree chart and Glaucoma.
His primary scientific interests are in Genetics, Genome-wide association study, Disease, Gene and Allele. His work often combines Genetics and TREM2 studies. His Genome-wide association study research incorporates elements of Missense mutation, Intraocular pressure, Open angle glaucoma, Linkage disequilibrium and Alzheimer's disease.
Jonathan L. Haines works mostly in the field of Disease, limiting it down to topics relating to Risk factor and, in certain cases, Cohort study and Haplotype. The Allele study combines topics in areas such as Exome sequencing, Apolipoprotein E and Genetic association. In his research, Genetic architecture and Genomics is intimately related to Locus, which falls under the overarching field of Single-nucleotide polymorphism.
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Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer's disease in late onset families
E. H. Corder;A. M. Saunders;W. J. Strittmatter;D. E. Schmechel.
Science (1993)
Finding the missing heritability of complex diseases
Teri A. Manolio;Francis S. Collins;Nancy J. Cox;David B. Goldstein.
Nature (2009)
Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease
R. Sherrington;E. I. Rogaev;Y. Liang;E. A. Rogaeva.
Nature (1995)
Effects of Age, Sex, and Ethnicity on the Association Between Apolipoprotein E Genotype and Alzheimer Disease: A Meta-analysis
Lindsay A. Farrer;L. Adrienne Cupples;Jonathan L. Haines;Bradley T Hyman.
JAMA (1997)
Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease
Jean-Charles Lambert;Jean-Charles Lambert;Jean-Charles Lambert;Carla A Ibrahim-Verbaas;Denise Harold;Adam C Naj.
Nature Genetics (2013)
Complement factor H variant increases the risk of age-related macular degeneration.
Jonathan L. Haines;Michael A. Hauser;Silke Schmidt;William K. Scott.
Science (2005)
Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis
Stephen Sawcer;Garrett Hellenthal;Matti Pirinen;Chris C. A. Spencer.
Nature (2011)
Mutations in the FUS/TLS gene on chromosome 16 cause familial amyotrophic lateral sclerosis.
T. J. Kwiatkowski;D. A. Bosco;D. A. Bosco;A. L. LeClerc;A. L. LeClerc;E. Tamrazian.
Science (2009)
Functional impact of global rare copy number variation in autism spectrum disorders
Dalila Pinto;Alistair T. Pagnamenta;Lambertus Klei;Richard Anney.
Nature (2010)
Genetic relationship between five psychiatric disorders estimated from genome-wide SNPs
S. Hong Lee;Stephan Ripke;Stephan Ripke;Benjamin M. Neale;Benjamin M. Neale;Stephen V. Faraone.
Nature Genetics (2013)
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