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Lindsay A. Farrer

Researcher at Boston University

Publications -  625
Citations -  56881

Lindsay A. Farrer is an academic researcher from Boston University. The author has contributed to research in topics: Genome-wide association study & Single-nucleotide polymorphism. The author has an hindex of 104, co-authored 572 publications receiving 49161 citations. Previous affiliations of Lindsay A. Farrer include McGill University & University of California, San Francisco.

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Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer's disease

Jean-Charles Lambert, +215 more
- 01 Dec 2013 - 
TL;DR: In addition to the APOE locus (encoding apolipoprotein E), 19 loci reached genome-wide significance (P < 5 × 10−8) in the combined stage 1 and stage 2 analysis, of which 11 are newly associated with Alzheimer's disease.
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Complement Factor H Polymorphism and Age-Related Macular Degeneration

TL;DR: In this paper, single-nucleotide polymorphisms were tested for association with AMD in two independent case-control populations and significant association was identified within the regulation of complement activation locus and was centered over a tyrosine-402 --> histidine-402 protein polymorphism in the gene encoding complement factor.
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Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease.

Adam C. Naj, +156 more
- 01 May 2011 - 
TL;DR: The Alzheimer Disease Genetics Consortium performed a genome-wide association study of late-onset Alzheimer disease using a three-stage design consisting of a discovery stage (stage 1), two replication stages (stages 2 and 3), and both joint analysis and meta-analysis approaches were used.
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Gene-wide analysis detects two new susceptibility genes for Alzheimer's disease.

Valentina Escott-Price, +194 more
- 12 Jun 2014 - 
TL;DR: The additional genes identified in this study, have an array of functions previously implicated in Alzheimer's disease, including aspects of energy metabolism, protein degradation and the immune system and add further weight to these pathways as potential therapeutic targets in Alzheimers disease.