Journal
JOURNAL OF NEUROCHEMISTRY
Volume 155, Issue 2, Pages 117-119Publisher
WILEY
DOI: 10.1111/jnc.15130
Keywords
-
Categories
Funding
- National Natural Science Foundation of China [81722016, 81801182]
- China Postdoctoral Science Foundation [2017M623041, 2019T120848]
- Key Research Projects of Sichuan Province [2018SZ0190]
- West China Hospital, Sichuan University [2018HXBH044]
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available