Abstract
Activation of microglial cells is involved in the inflammatory component of Alzheimer's disease (AD), and it may be triggered by infectious pathogens. CD14, a receptor upregulated in activated microglia, plays a central role in innate immunity through recognition of bacterial lipopolysaccharide and initiation of inflammatory response. A polymorphism in the promoter region (−260) of the CD14 receptor has been found to be related to increased risk of bacterial infections and inflammatory diseases such as atherosclerosis. In a case-control study utilizing a clinically well-defined group of 310 sporadic AD patients and 310 control subjects, we investigated whether the CD14 (−260) polymorphism might be responsible for susceptibility to AD, and we also examined the combined gene effects between CD14 and APOE and several other proinflammatory cytokine genes. The current study does not demonstrate an association between CD14 (−260) polymorphism and AD, neither through an independent effect nor through interaction with APOE ɛ4 allele or interleukin (IL)-1A, IL-6, IL-8, tumor necrosis factor (TNF)-α, and intercellular adhesion molecule-1 polymorphisms.
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