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Towards Understanding the Molecular Basis of Parkinson’s Disease: Cell-based Model of Mitophagy and Aggresome Accumulation

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Wayne F. Patton
Enzo Life Sciences, Farmingdale, New York, USA

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INTRODUCTION

Parkinson’s disease (PD) is an incapacitating, age-related neurodegenerative disease, affecting all populations, with approximately 1.5 million confirmed cases in the United States alone. Data from various studies of genes associated with hereditary disease, toxicology studies using animal models/in vitro models and also patient-based studies have implicated compromised protein turnover relating to the ubiquitin-proteasome system (UPS) and autophagy-lysosome pathway (ALP), as well as diminished mitochondrial activity in the most common idiopathic forms of the disease. Mutations in the Parkin gene are a primary cause of autosomal recessive juvenile PD. Parkin functions as an E3 ligase that ubiquitinylates α-synuclein, the primary aggregated protein associated with the neurotoxic accumulation in Lewy bodies. Parkin also interacts with and ubiquitinylates depolarized mitochondria, promoting their clearance by mitophagy. Cell-based assays relevant to monitoring aspects of PD are presented, including aberrant aggresome formation, mitochondrial depolarization, ubiquitinylation and mitophagy. The described assays should contribute to the understanding of regulatory pathways controlling mitophagy and Lewy body formation, aiding in the characterization of various human neuropathological disorders, including PD.

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