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对723对晚发性阿尔茨海默病患病亲属进行全基因组连锁分析。

Genome-wide linkage analysis of 723 affected relative pairs with late-onset Alzheimer's disease.

作者信息

Hamshere Marian L, Holmans Peter A, Avramopoulos Dimitrios, Bassett Susan S, Blacker Deborah, Bertram Lars, Wiener Howard, Rochberg Nan, Tanzi Rudolph E, Myers Amanda, Wavrant-De Vrièze Fabienne, Go Rodney, Fallin Daniele, Lovestone Simon, Hardy John, Goate Alison, O'Donovan Michael, Williams Julie, Owen Michael J

机构信息

Biostatistics and Bioinformatics Unit, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.

出版信息

Hum Mol Genet. 2007 Nov 15;16(22):2703-12. doi: 10.1093/hmg/ddm224. Epub 2007 Aug 27.

Abstract

Previous attempts to identify genetic loci conferring risk for late-onset Alzheimer's disease (LOAD) through linkage analysis have observed some regions of linkage in common. However, due to the sometimes-considerable overlap between the samples, some of these reports cannot be considered to be independent replications. In order to assess the strength of the evidence for linkage and to obtain the best indication of the location of susceptibility genes, we have amalgamated three large samples to give a total of 723 affected relative pairs (ARPs). Multipoint, model-free ARP linkage analysis was performed. Genome-wide significant evidence for linkage was observed on 10q21.2 (LOD=3.3) and genome-wide suggestive evidence was observed on 9q22.33 (LOD=2.5) and 19q13.32 (LOD=2.0). One further region on 9p21.3 was identified with an LOD score>1. We observe no evidence to suggest that more than one locus is responsible for the linkage to 10q21.2, although this linked region may harbour more than one susceptibility gene. Evidence of allele-sharing heterogeneity between the original collection sites was observed on chromosome 9 but not on chromosome 10 or 19. Evidence for an interaction was observed between loci on chromosomes 10 and 19. Where samples overlapped, the genotyping consistency was high, estimated to average at 97.3%. Our large-scale linkage analysis consolidates clear evidence for a susceptibility locus for LOAD on 10q21.2.

摘要

以往通过连锁分析来确定晚发性阿尔茨海默病(LOAD)风险相关基因座的尝试,发现了一些共同的连锁区域。然而,由于样本之间有时存在相当大的重叠,其中一些报告不能被视为独立的重复验证。为了评估连锁证据的强度,并获得对易感基因位置的最佳指示,我们合并了三个大样本,总共得到723对患病亲属对(ARP)。进行了多点、无模型的ARP连锁分析。在10q21.2观察到全基因组显著的连锁证据(LOD = 3.3),在9q22.33(LOD = 2.5)和19q13.32(LOD = 2.0)观察到全基因组提示性连锁证据。在9p21.3还确定了另一个LOD得分>1的区域。我们没有发现证据表明有多个基因座与10q21.2的连锁有关,尽管这个连锁区域可能包含不止一个易感基因。在9号染色体上观察到了原始收集位点之间等位基因共享异质性的证据,但在10号和19号染色体上未观察到。在10号和19号染色体上的基因座之间观察到了相互作用的证据。在样本重叠的地方,基因分型一致性很高,估计平均为97.3%。我们的大规模连锁分析巩固了10q21.2上存在LOAD易感基因座的明确证据。

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