Iron-induced cytotoxicity mediated by endolysosomal TRPML1 channels is reverted by TFEB

ABSTRACT: Increased brain iron content has been consistently reported in sporadic Parkinson’s disease (PD) patients, and an increase in cytosolic free iron is known to cause oxidative stress and cell death. However, whether iron also accumulates in susceptible brain areas in humans or in mouse models of familial PD remains unknown. In addition, whilst the lysosome functions as a critical intracellular iron storage organelle, little is known about the mechanisms underlying lysosomal iron release and how this process is influenced by lysosome biogenesis and/or lysosomal exocytosis. Here, we report an increase in brain iron content also in PD patients due to the common G2019S-LRRK2 mutation as compared to healthy age-matched controls, whilst differences in iron content are not observed in G2019S-LRRK2

SUBMITTER: Fernandez B 

PROVIDER: S-EPMC9755144 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature