Cu^II (atsm) inhibits ferroptosis: Implications for treatment of neurodegenerative disease.

ABSTRACT:

Background and purpose

Diacetyl-bis(4-methyl-3-thiosemicarbazonato)copper^II (Cu^II (atsm)) ameliorates neurodegeneration and delays disease progression in mouse models of amyotrophic lateral sclerosis (ALS) and Parkinson's disease (PD), yet the mechanism of action remains uncertain. Promising results were recently reported for separate Phase 1 studies in ALS patients and PD patients. Affected tissue in these disorders shares features of elevated Fe, low glutathione and increased lipid peroxidation consistent with ferroptosis, a novel form of regulated cell death. We therefore evaluated the ability of Cu^II (atsm) to inhibit ferroptosis.

Experimental approach

Ferroptosis was induced in neuronal cell models by inhibition of glutathione peroxidase

SUBMITTER: Southon A 

PROVIDER: S-EPMC7012947 | biostudies-literature | 2020 Feb

REPOSITORIES: biostudies-literature