TNF-α 308 G/A and 238 G/A promoter polymorphisms and sporadic Parkinson's disease in an Italian cohort

The etiology of sporadic Parkinson's disease is (PD) still not understood but it is believed that a complex interplay between environmental and genetic factors could trigger the pathology. Pro-inflammatory TNF-alpha is released by activated microglia and is up-regulated in the brain and cerebrospinal fluid of PD patients; TNF-alpha modulates neuroinflammation and can activate the molecular mechanisms that lead to neurotoxicity and neuronal death. We analyzed two functional SNPs within the TNF-alpha gene promoter (rs361525 and rs1800629) in 354 Italian PD patients and 443 healthy controls (HC). In our cohort of patients, no significant associations could be observed between rs361525 and rs1800629 SNPs and either PD onset risk or PD-associated clinical parameters including age at onset of fluctuations, UPDRS-ME (Unified Parkinson Disease Rating Scale-Motor Examination), Schwab & England, Hohen & Yahr stage scale, and MMSE (Mini-Mental State Examination) score. Conflicting results on the role played by TNF-alpha rs1800629 SNP on PD onset risk are present in the literature. We could not find any association between TNF-alpha rs361525 and rs1800629 and PD.