Variation in the urokinase-plasminogen activator gene does not explain the chromosome 10 linkage signal for late onset AD.
Myers AJ., Marshall H., Holmans P., Compton D., Crook RJ., Mander AP., Nowotny P., Smemo S., Dunstan M., Jehu L., Wang JC., Hamshere M., Morris JC., Norton J., Chakraventy S., Tunstall N., Lovestone S., Petersen R., O'Donovan M., Jones L., Williams J., Owen MJ., Hardy J., Goate A.
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.