Objective: The present study was initiated to evaluate a possible relationship between CD14 monocyte receptor genetic polymorphism and the risk of Parkinson's disease (PD).
Background: Inflammatory processes have been postulated to play a role in the pathogenesis of PD. The C(Ϫ260) 3 T polymorphism in the promoter of the CD14 gene (pCD14) has been proven to cause individuals to be genetically susceptible to chronic inflammatory disorders.
Methods: A case-control study was carried out to examine the association of the pCD14 polymorphism between 200 patients with clinical definite sporadic PD and 200 controls, matched by age and sex. The CIT polymorphism of the pCD14 was identified by conventional polymerase chain reaction and fragment restriction length polymorphism resulting in three genotypes (CC/TT homozygotes and CT heterozygote).
Results: Although the frequencies of both the homozygote TT genotype (CD14-TT) and T allele (CD14-T) of the pCD14 polymorphism in the PD patients were higher than that in the controls, these differences did not reach significant levels (P ϭ 0.579 and 0.303, respectively). Analysis of the differences in the pCD14 polymorphism stratified by gender revealed that there was a significant difference in CD14-T allele in the female PD patients compared with control subjects (OR ϭ 1.262, 95% CI ϭ 1.006 -1.583, 2 ϭ 4.292, P ϭ 0.038). Individuals with homozygote CD14-TT genotype were also detected significantly more frequently in female PD patients compared with control subjects (95% CI ϭ 1.025-1.599, 2 ϭ 4.881, P ϭ 0.027). A multiple logistic regression analysis of the presence of the CD14-TT genotype and data on putative risk factors for developing PD confirmed that the homozygote CD14-TT genotype was an independent risk factor for PD (OR ϭ 2.276, 95% CI ϭ 1.084 -4.780, P ϭ 0.030).
Conclusion: Results of our study reveal a genetic susceptibility to PD in female individuals by the CD14 monocyte receptor. Furthermore, the result supports the hypothesis that inflammation may be involved in the pathogenesis of PD, particularly in female individuals.