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No evidence that extended tracts of homozygosity are associated with Alzheimer's disease

Research output: Contribution to journalArticle

Rebecca Sims, Sarah Dwyer, Denise Harold, Amy Gerrish, Paul Hollingworth, Jade Chapman, Nicola Jones, Richard Abraham, Dobril Ivanov, Jaspreet Singh Pahwa, Valentina Moskvina, Kimberley Dowzell, Charlene Thomas, Alexandra Stretton, Simon Lovestone, John Powell, Petroula Proitsi, Michelle K Lupton, Carol Brayne, David C Rubinsztein & 29 more Michael Gill, Brian Lawlor, Aoibhinn Lynch, Kevin Morgan, Kristelle S Brown, Peter A Passmore, David Craig, Bernadette McGuiness, Stephen Todd, Janet A Johnston, Clive Holmes, David Mann, A David Smith, Seth Love, Patrick G Kehoe, John Hardy, Simon Mead, Nick Fox, Martin Rossor, John Collinge, Gill Livingston, Nicholas J Bass, Hugh Gurling, Andrew McQuillin, Lesley Jones, Peter A Holmans, Michael O'Donovan, Michael J Owen, Julie Williams

Original languageEnglish
Pages (from-to)764-71
Number of pages8
JournalAmerican Journal of Medical Genetics. Part B: Neuropsychiatric Genetics
Volume156B
Issue number7
DOIs
Publication statusPublished - Dec 2011

King's Authors

Abstract

We sought to investigate the contribution of extended runs of homozygosity in a genome-wide association dataset of 1,955 Alzheimer's disease cases and 955 elderly screened controls genotyped for 529,205 autosomal single nucleotide polymorphisms. Tracts of homozygosity may mark regions inherited from a common ancestor and could reflect disease loci if observed more frequently in cases than controls. We found no excess of homozygous tracts in Alzheimer's disease cases compared to controls and no individual run of homozygosity showed association to Alzheimer's disease.

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