Genetic analysis of interleukin-1A C(-889)T polymorphism with Alzheimer disease
Ji-Liang Hu1, Gang Li, De-Xiang Zhou
1Neurosurgery Department, Key Laboratory on Brain Function Repair and Regeneration of Guangdong, Neurosurgery Institute, Affiliated Zhujiang Hospital of Southern Medical University, Guangzhou, China.
Abstract:
Neuroinflammation has been implicated in the etiology of Alzheimer's disease (AD). Many studies have suggested that C(-889) T promoter polymorphism in one of the proinflammatory cytokine interleukin-1 (IL-1) encoding gene IL-1A may be associated with AD pathogenesis. To determine whether the polymorphism contributes to the risk for late-onset AD (LOAD) in Chinese, we carried out our investigation in 344 sporadic LOAD patients and 224 healthy controls. No statistical significant association was obtained between IL-1A C(-889) T polymorphism and LOAD and no statistical difference was found between cases and controls after stratification for apolipoprotein E allele 4 (APOE epsilon4) status. The results reveal that it is not likely that the IL-1A C(-889) T polymorphism is involved in AD pathogenesis in the Chinese population. Further studies of the associations between other IL-1A genetic polymorphisms and AD should be performed in a larger population and biologic functional analysis of IL-1A gene is required to verify the underlying roles of IL-IA in LOAD.
Related Concept Videos
Pharmacogenetics of Drug Targets: β₂-Adrenergic Receptors, Apo E, Thymidylate Synthase
Alzheimer Disease ll: Pathophysiology
Alzheimer Disease l: Introduction
Single Nucleotide Polymorphisms-SNPs


