Genetic analysis of interleukin-1A C(-889)T polymorphism with Alzheimer disease.

Cell Mol Neurobiol

Neurosurgery Department, Key Laboratory on Brain Function Repair and Regeneration of Guangdong, Neurosurgery Institute, Affiliated Zhujiang Hospital of Southern Medical University, Guangzhou, China.

Published: February 2009

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.

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Source
http://dx.doi.org/10.1007/s10571-008-9299-5DOI Listing

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