Lack of association between IL-1β, TNF-α, and IL-10 gene polymorphisms and sporadic Parkinson's disease in an Italian cohort.

OBJECTIVE

There is increasing evidence suggesting that neuroinflammation and microglia activation may play important roles in the pathway leading to neuronal cell death in Parkinson's disease (PD). Chronic activation of microglia may cause neuronal damage through the release of potentially cytotoxic molecules, such as pro-inflammatory cytokines. Different functional promoter polymorphisms within genes coding pro- or anti-inflammatory cytokines involved in the immune reactions in the brain might influence the risk of developing PD or the age of disease onset.

AIM

To investigate the interleukin (IL)-1β-511, tumor necrosis factor alpha (TNF-α)-308, and interleukin (IL)-10-1082 gene polymorphisms as susceptibility factors for PD.

METHODS

We analyzed genotype and allele distributions of these polymorphisms in 146 Italian patients with PD and 156 healthy controls.

RESULTS

None of the polymorphisms we investigated was found to be associated with PD or with age of disease onset. No significant differences between patients with PD and controls were found as regards the concomitant presence of variant alleles in the three polymorphisms studied. We found that only the combined genotype TNF-α-308GG/IL-1β-511T+ is associated with a decreased risk of PD.

CONCLUSION

Our results indicate that the cytokine gene polymorphisms we investigated are not related to the development of PD in the Italian population; further studies are warranted to clarify the role of the TNF-α-308GG/IL-1β-511T+ combined genotype.