The chemokine receptor CCR5-Δ32 gene mutation is not protective against Alzheimer's disease

被引:24
作者
Combarros, O [1 ]
Infante, J
Llorca, J
Peña, N
Fernández-Viadero, C
Berciano, J
机构
[1] Univ Cantabria, Univ Hosp Marques Valdecilla, Serv Neurol, Santander 39008, Spain
[2] Univ Cantabria, Sch Med, Div Prevent Med, Santander 39008, Spain
[3] RTE Santander, Consejeria Sanidad, Santander, Spain
关键词
Alzheimer's disease; CCR5; chemokine; polymorphism;
D O I
10.1016/j.neulet.2004.05.058
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Chronic local inflammatory reaction involving reactive microglia is one of the major pathological events in Alzheimer's disease (AD). There is growing evidence that the chemokine receptor CCR5 is up-regulated in AD brain and plays a role in the recruitment and accumulation of microglia in senile plaques. A 32-base pair deletion in the CCR5 gene (CCR5-Delta32 mutant allele) confers resistance to HIV-1 infection by preventing expression of the receptor on the cell surface. Several other reports have shown a similar protective effect of CCR5-Delta32 mutation towards certain chronic inflammatory diseases. Given the potential importance of CCR5 in brain inflammation, we hypothesized that individuals carrying the CCR5-Delta32 allele would show a reduced risk of AD. So, we performed a case-control study in 376 Spanish AD patients and 369 healthy controls. The frequency of the CCR5-Delta32 allele in our AD sample was 7.8%, not significantly different from our control sample group (5.8%). The present study indicates that the CCR5-Delta32 allele is not a preventive factor for AD. (C) 2004 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:312 / 314
页数:3
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