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. © 2003 Wiley-Liss, Inc.
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Myers, A. J., Marshall, H., Holmans, P., Compton, D., Crook, R. J. P., Mander, A. P., … 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
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