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Iron Dysregulation in Parkinson's Disease: Focused on the Autophagy-Lysosome Pathway.

Abstract：

:Parkinson's disease (PD) is the second most common neurodegenerative disease and is characterized by dopaminergic neuron loss in the substantia nigra pars compacta (SNpc). Although both iron accumulation and a defective autophagy-lysosome pathway contribute to the pathological development of PD, the connection between these two causes is poorly documented. The autophagy-lysosome pathway not only responds to regulation by iron chelators and channels but also participates in cellular iron recycling through the degradation of ferritin and other iron-containing components. Previously, ferritin has been posited to be the bridge between iron accumulation and autophagy impairment in PD. In addition, iron directly interacts with α-synuclein in Lewy bodies, which are primarily digested through the autophagy-lysosome pathway. These findings indicate that some link exists between iron deposition and autophagy impairment in PD. In this review, the basic mechanisms of the autophagy-lysosome pathway and iron trafficking are introduced, and then their interaction under physiological conditions is explained. Finally, we finish by discussing the dysfunction of iron deposition and autophagy in PD, as well as their potential relationship, which will provide some insight for further study.

journal_name

ACS Chem Neurosci

journal_title

ACS chemical neuroscience

authors

Chen LL,Huang YJ,Cui JT,Song N,Xie J

doi

10.1021/acschemneuro.8b00390

subject

Has Abstract

pub_date

2019-02-20 00:00:00

pages

863-871

issue

2

issn

1948-7193

journal_volume

10

pub_type

杂志文章,评审

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