Role of Deubiquitinases in Parkinson’s Disease—Therapeutic Perspectives

Pernille Y. Ø. Nielsen, Justyna Okarmus, Morten Meyer*


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Parkinson’s disease (PD) is a neurodegenerative disorder that has been associated with mitochondrial dysfunction, oxidative stress, and defects in mitophagy as well as α-synuclein-positive inclusions, termed Lewy bodies (LBs), which are a common pathological hallmark in PD. Mitophagy is a process that maintains cellular health by eliminating dysfunctional mitochondria, and it is triggered by ubiquitination of mitochondrial-associated proteins—e.g., through the PINK1/Parkin pathway—which results in engulfment by the autophagosome and degradation in lysosomes. Deubiquitinating enzymes (DUBs) can regulate this process at several levels by deubiquitinating mitochondrial substrates and other targets in the mitophagic pathway, such as Parkin. Moreover, DUBs can affect α-synuclein aggregation through regulation of degradative pathways, deubiquitination of α-synuclein itself, and/or via co-localization with α-synuclein in inclusions. DUBs with a known association to PD are described in this paper, along with their function. Of interest, DUBs could be useful as novel therapeutic targets against PD through regulation of PD-associated defects.

Udgave nummer4
Antal sider30
StatusUdgivet - feb. 2023

Bibliografisk note

Funding Information:
The study was supported by the Danish Parkinson Foundation, and the Faculty of Health Sciences at the University of Southern Denmark.


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