4.5 Editorial Material

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 https://doi.org/10.1111/jnc.15107

Journal

JOURNAL OF NEUROCHEMISTRY
Volume 155, Issue 2, Pages 117-119

Publisher

WILEY
DOI: 10.1111/jnc.15130

Keywords

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Funding

  1. National Natural Science Foundation of China [81722016, 81801182]
  2. China Postdoctoral Science Foundation [2017M623041, 2019T120848]
  3. Key Research Projects of Sichuan Province [2018SZ0190]
  4. West China Hospital, Sichuan University [2018HXBH044]

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

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