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Review

Interaction between Parkin and α-Synuclein in PARK2-Mediated Parkinson’s Disease

1
Department of Neurobiology Research, Institute of Molecular Medicine, University of Southern Denmark, 5000 Odense, Denmark
2
Department of Neurology, Odense University Hospital, 5000 Odense, Denmark
3
Department of Clinical Research, University of Southern Denmark, 5000 Odense, Denmark
4
BRIDGE—Brain Research Inter-Disciplinary Guided Excellence, Department of Clinical Research, University of Southern Denmark, 5000 Odense, Denmark
*
Author to whom correspondence should be addressed.
Cells 2021, 10(2), 283; https://doi.org/10.3390/cells10020283
Received: 29 December 2020 / Revised: 25 January 2021 / Accepted: 26 January 2021 / Published: 31 January 2021
(This article belongs to the Collection Feature Papers in ‘Cellular Pathology’)
Parkin and α-synuclein are two key proteins involved in the pathophysiology of Parkinson’s disease (PD). Neurotoxic alterations of α-synuclein that lead to the formation of toxic oligomers and fibrils contribute to PD through synaptic dysfunction, mitochondrial impairment, defective endoplasmic reticulum and Golgi function, and nuclear dysfunction. In half of the cases, the recessively inherited early-onset PD is caused by loss of function mutations in the PARK2 gene that encodes the E3-ubiquitin ligase, parkin. Parkin is involved in the clearance of misfolded and aggregated proteins by the ubiquitin-proteasome system and regulates mitophagy and mitochondrial biogenesis. PARK2-related PD is generally thought not to be associated with Lewy body formation although it is a neuropathological hallmark of PD. In this review article, we provide an overview of post-mortem neuropathological examinations of PARK2 patients and present the current knowledge of a functional interaction between parkin and α-synuclein in the regulation of protein aggregates including Lewy bodies. Furthermore, we describe prevailing hypotheses about the formation of intracellular micro-aggregates (synuclein inclusions) that might be more likely than Lewy bodies to occur in PARK2-related PD. This information may inform future studies aiming to unveil primary signaling processes involved in PD and related neurodegenerative disorders. View Full-Text
Keywords: familial Parkinson’s disease; PARK2; parkin; α-synuclein; Lewy bodies familial Parkinson’s disease; PARK2; parkin; α-synuclein; Lewy bodies
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MDPI and ACS Style

Madsen, D.A.; Schmidt, S.I.; Blaabjerg, M.; Meyer, M. Interaction between Parkin and α-Synuclein in PARK2-Mediated Parkinson’s Disease. Cells 2021, 10, 283. https://doi.org/10.3390/cells10020283

AMA Style

Madsen DA, Schmidt SI, Blaabjerg M, Meyer M. Interaction between Parkin and α-Synuclein in PARK2-Mediated Parkinson’s Disease. Cells. 2021; 10(2):283. https://doi.org/10.3390/cells10020283

Chicago/Turabian Style

Madsen, Daniel Aghaie, Sissel Ida Schmidt, Morten Blaabjerg, and Morten Meyer. 2021. "Interaction between Parkin and α-Synuclein in PARK2-Mediated Parkinson’s Disease" Cells 10, no. 2: 283. https://doi.org/10.3390/cells10020283

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