Iron promotes the clearance of α-synuclein: An Editorial for 'H63D variant of the homeostatic iron regulator (HFE) gene alters α-synuclein expression, aggregation, and toxicity" on page 177

Abstract

Both elevated iron and α-synuclein (α-syn) aggregates are neuropathological hallmarks of Parkinson's disease (PD). It has been previously shown that iron promotes α-synuclein aggregation, and α-synuclein dysfunction impairs iron metabolism. In their latest work, Kim et al. have shown that the H63D variant of the homeostatic iron regulator (HFE) facilitates α-syn degradation via REDD1-mediated autophagy. Mice with the H63D variant of HFE were protected against α-syn toxicity. These results may shed light on recent clinical studies of PD using iron chelation therapy.