Background There were some papers published in the Jonmal of Science, December 2000 suggesting that one or more important susceptibility genes for late onset Alzheimer＇s disease （LOAD） were located on the long arm ...Background There were some papers published in the Jonmal of Science, December 2000 suggesting that one or more important susceptibility genes for late onset Alzheimer＇s disease （LOAD） were located on the long arm of chromosome 10. Linkage analysis showed maximum lod score close to D10S1225 loci, which indicated the loci might contribute to the etiology of Alzheimer＇s disease （AD）. Methods Fifty-nine LOAD patients and 107 controls were recruited. Apolipoprotein E （ApoE） genotypes were determined by reverse dot blotting hybridization assay. The D10S1225 was genotyped by 12% nondenaturing polyacrylamide gels electrophoresis and analyzed by silver staining. Statistical analysis was used to compare genotype and allele distributions between LOAD group and control group for APOE and D10S1225 polymorphisms. Results APOE ε4 was significantly higher in LOAD group in comparison with the control group（X^2=6.530, P=0.011）. Seven different alleles of D10S1225 have been identified. The length of these gene fragments were 178 bp, 181 bp, 184 bp, 187 bp, 190 bp, 193 bp, and 196 bp, respectively. A total of 21 different genotypes were observed. There was no relationship between D10S1225 polymorphism and LOAD （X^2=4.488, P〉0.05）. Conclusion This study suggests that ApoEεA is a risk factor for LOAD, however, the results indicated that there is not any possible linkage for disequilibria with a nearby AD risk gene near D10S1225.展开更多
基金This study was supported by a grant from the Natural Sciences Foundation of China (No. 30470904).
文摘Background There were some papers published in the Jonmal of Science, December 2000 suggesting that one or more important susceptibility genes for late onset Alzheimer＇s disease （LOAD） were located on the long arm of chromosome 10. Linkage analysis showed maximum lod score close to D10S1225 loci, which indicated the loci might contribute to the etiology of Alzheimer＇s disease （AD）. Methods Fifty-nine LOAD patients and 107 controls were recruited. Apolipoprotein E （ApoE） genotypes were determined by reverse dot blotting hybridization assay. The D10S1225 was genotyped by 12% nondenaturing polyacrylamide gels electrophoresis and analyzed by silver staining. Statistical analysis was used to compare genotype and allele distributions between LOAD group and control group for APOE and D10S1225 polymorphisms. Results APOE ε4 was significantly higher in LOAD group in comparison with the control group（X^2=6.530, P=0.011）. Seven different alleles of D10S1225 have been identified. The length of these gene fragments were 178 bp, 181 bp, 184 bp, 187 bp, 190 bp, 193 bp, and 196 bp, respectively. A total of 21 different genotypes were observed. There was no relationship between D10S1225 polymorphism and LOAD （X^2=4.488, P〉0.05）. Conclusion This study suggests that ApoEεA is a risk factor for LOAD, however, the results indicated that there is not any possible linkage for disequilibria with a nearby AD risk gene near D10S1225.
