4.4 Article

Single nucleotide polymorphisms in the toll-like receptor 2 (TLR2) gene are associated with sporadic Parkinson's disease in the North-eastern Han Chinese population

Journal

NEUROSCIENCE LETTERS
Volume 656, Issue -, Pages 72-76

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2017.07.014

Keywords

Toll-like receptor 2 (TLR2); Parkinson's disease (PD); Single nucleotide polymorphisms (SNPs)

Categories

Funding

  1. Chinese National Human Genome Center, Beijing
  2. Natural Science Foundation of China [81571225]

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Growing evidences suggested that inflammatory process played a critical role in the pathogenesis of Parkinson's disease (PD). Given that TLR2 has been implicated in the perpetuation of inflammatory responses in the central nervous system (CNS), we investigated the association between two genetic variants (rs3804099 and rs3804100) of TLR2 and sporadic PD in Han Chinese population. 395 Han Chinese sporadic PD patients and 413 healthy age and gender-matched controls were genotyped using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. The sporadic PD patients showed a higher T allele frequency than the healthy-matched control (p = 0.019). Furthermore rs3804099 dominate model TT versus (vs.) TC + CC increase the risk of sporadic PD (OR =1.376, 95%CI = 1.043-1.814,p = 024). From the subgroup analysis, the variant allele T of rs3804099 was higher in sporadic PD cases (73.1%) than in controls (67.4%) in the late-onset cohort. Meanwhile rs3804099 revealed significant association in dominant model: Subjects with TT genotypes vs. those with TC + CC genotype showed evident significant in late-onset cohort (LOPD OR = 1.417, 95%Cl = 1.051-1.911, p = 022). In contrast, allele frequencies at rs3804100 were similar between patients and controls. Taken together, this study reveals that polymorphism of TLR2 locus is associated with risk of sporadic PD in the North-eastern part of Han Chinese population. Further studies are required to evaluate the association. (C) 2017 Elsevier B.V. All rights reserved.

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