Variation in the Urokinase-Plasminogen Activator Gene Does Not Explain the Chromosome 10 Linkage Signal for Late Onset AD

Amanda J. Myers, Helen Marshall, Peter Holmans, Danielle Compton, Richard J.P. Crook, Adrian P. Mander, Petra Nowotny, Scott Smemo, Melanie Dunstan, Luke Jehu, Jen C. Wang, Marian Hamshere, John C. Morris, Joanne Norton, Sumi Chakraventy, Nigel Tunstall, Simon Lovestone, Ronald Petersen, Michael O'Donovan, Lesley JonesJulie Williams, Michael J. Owen, John Hardy, Alison Goate

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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 Aβ42 levels suggesting that a single locus may influence risk for AD by elevating plasma Aβ42 [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.

Original languageEnglish
Pages (from-to)29-37
Number of pages9
JournalAmerican Journal of Medical Genetics - Neuropsychiatric Genetics
Volume124 B
Issue number1
DOIs
StatePublished - Jan 1 2004

Keywords

  • Alzheimer disease
  • Association study
  • Candidate gene
  • PLAU
  • Urokinase-plasminogen activator

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    Myers, A. J., Marshall, H., Holmans, P., Compton, D., Crook, R. J. P., Mander, A. P., Nowotny, P., Smemo, S., Dunstan, M., Jehu, L., Wang, J. C., Hamshere, M., Morris, J. C., Norton, J., Chakraventy, S., Tunstall, N., Lovestone, S., Petersen, R., O'Donovan, M., ... Goate, A. (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 - Neuropsychiatric Genetics, 124 B(1), 29-37. https://doi.org/10.1002/ajmg.b.20036