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Variation in the urokinase-plasminogen activator gene does not explain the chromosome 10 linkage signal for late onset AD

Myers, Amanda J., Marshall, Helen, Holmans, Peter Alan, Compton, Danielle, Crook, Richard J.P., Mander, Adrian P., Nowotny, Petra, Smemo, Scott, Dunstan, Melanie, Jehu, Luke, Wang, Jen C., Hamshere, Marian Lindsay, Morris, John C., Norton, Joanne, Chakraventy, Sumi, Tunstall, Nigel, Lovestone, Simon, Petersen, Ronald, O'Donovan, Michael Conlon, Jones, Lesley, Williams, Julie, Owen, Michael John, Hardy, John and Goate, Alison 2004. Variation in the urokinase-plasminogen activator gene does not explain the chromosome 10 linkage signal for late onset AD. American Journal of Medical Genetics 124B (1) , pp. 29-37. 10.1002/ajmg.b.20036

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Abstract

Linkage studies indicate that the same region of chromosome 10 contains a risk locus for late onset Alzheimer disease (LOAD) and a QTL for plasma Abeta42 levels suggesting that a single locus may influence risk for AD by elevating plasma Abeta42 [Ertekin-Taner et al., 2000; Myers et al., 2000]. A strong positional and biological candidate is the urokinase-plasminogen activator (PLAU) gene. Eight polymorphisms spanning the entire gene were examined using case control (CC) and family-based association methods. No association was observed by any method making it unlikely that variation in PLAU explains our linkage data.

Item Type: Article
Date Type: Publication
Status: Published
Schools: MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG)
Medicine
Neuroscience and Mental Health Research Institute (NMHRI)
Subjects: R Medicine > R Medicine (General)
Publisher: Wiley
ISSN: 0148-7299
Last Modified: 28 Jun 2019 02:42
URI: http://orca.cf.ac.uk/id/eprint/81794

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