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Background  Toll-like receptors (TLRs), as major innate immune mediators, may be involved in clearance of cerebral amyloid-β (Aβ) deposits. Recently, a novel TLR9 signaling pathway has been uncovered, which is functionally associated with the immune inflammatory response and reducing Aβ burden in Alzheimer’s disease (AD) mice. Therefore,  TLR9  might represent a reasonable functional candidate gene for AD.    Findings  Our study investigated 1,133 sporadic late-onset AD (LOAD) and 1,159 healthy controls matched for sex and age in a large Han Chinese population. One selected functional rs187084 polymorphism within the  TLR9  gene was genotyped by polymerase chain reaction-ligase detection reaction in a case–control associated study. The  TLR9  rs187084 variant homozygote GG was significantly associated with a decreased LOAD risk after adjusting for age, gender, and ApoE ϵ4 status by logistic regression analysis ( P  = 0.035). Our result showed significant evidence of the interaction of ApoE ϵ4 with rs187084. When we further stratified our data by the ApoE ϵ4 status, we detected significant differences in the genotype and allele distributions of rs187084 between LOAD patients and controls in ApoE ϵ4 carriers ( P  < 0.001,  P  = 0.003, respectively). Moreover, we examined  TLR9  expression in peripheral blood monocytes by flow cytometry, and the GG genotype of the  TLR9  rs187084 polymorphism was associated with a higher  TLR9  expression than two other genotypes in LOAD patients.    Conclusion  Our findings support the hypothesis that the  TLR9  polymorphism may modify LOAD risk in the Han Chinese population.

Toll-like receptor 9 promoter polymorphism is associated with decreased risk of Alzheimer’s disease in Han Chinese