Tuesday 14 April 2015

The association between the C282Y and H63D polymorphisms of HFE gene and the risk of Parkinson's disease: A meta-analysis

Iron is an important factor in a number of neurodegenerative diseases including the rare NBIA (neurodegeneration with brain iron accumulation) disorders. In recent years, a potential role for iron in Parkinson's has emerged and even prompted clinical trials of drugs that alter body iron levels. Here are data suggesting a certain gene variant, important in iron handling, appears to protect against Parkinson's...

Iron (source Wikipedia)


Neurosci Lett. 2015 Apr 8. pii: S0304-3940(15)00283-9. doi: 10.1016/j.neulet.2015.04.010. [Epub ahead of print]
Xia J, Xu H, Jiang H, Xie J.


Impaired brain iron homeostasis has been considered as an important mechanism in Parkinson's diseases (PD). There are indications that C282Y and H63D polymorphisms of HFE genes involved in iron metabolism might contribute to the pathogenesis of PD in some cases. However, the investigation of the relationship between PD and the two polymorphisms had produced contradictory results. We performed a meta-analysis to assess the C282Y and H63D polymorphisms of HFE in PD susceptibility. PubMed, EMBASE and Web of Science were systematically searched to identify relevant researches. The strict selection criteria and exclusion standard were applied. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of associations. A fixed-effect or random-effect model was selected, depending on the results of the heterogeneity test. Fifteen studies were included in the meta-analysis (eight studies with 1,631 cases and 4,548 controls for C282Y; seven studies with 1,192 cases and 4,065 controls for H63D). For the C282Y polymorphism, significant associations were observed in the Recessive model (YY vs CY+CC: OR=0.22, 95% CI=0.09-0.57, P=0.002). This indicated that the C282Y polymorphism in HFE might be a potential protective factor for PD. However, no significant associations were found for any genetic model for the H63D polymorphism, suggesting that the H63D polymorphism might not be associated with PD.

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