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

Am J Med Genet B Neuropsychiatr Genet. 2004 Jan 1;124B(1):29-37. doi: 10.1002/ajmg.b.20036.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Alleles
  • Alzheimer Disease / genetics*
  • Alzheimer Disease / pathology
  • Case-Control Studies
  • Chromosomes, Human, Pair 10 / genetics*
  • Female
  • Gene Frequency
  • Genetic Linkage
  • Genotype
  • Haplotypes
  • Humans
  • Male
  • Polymorphism, Genetic
  • Urokinase-Type Plasminogen Activator / genetics*

Substances

  • Urokinase-Type Plasminogen Activator