Abstract
Parkinson’s disease (PD) is the most common movement disorder with motor and nonmotor signs. The current therapeutic regimen for PD is mainly symptomatic as the etio-pathophysiology has not been fully elucidated. A variety of animal models has been generated to study different aspects of the disease for understanding the pathogenesis and therapeutic development. The disease model can be generated through neurotoxin-based or genetic-based approaches in a wide range of animals such as non-human primates (NHP), rodents, zebrafish, Caenorhabditis (C.) elegans, and drosophila. Cellular-based disease model is frequently used because of the ease of manipulation and suitability for large-screen assays. In neurotoxin-induced models, chemicals such as 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), rotenone, and paraquat are used to recapitulate the disease. Genetic manipulation of PD-related genes, such as α-Synuclein(SNCA), Leucine-rich repeat kinase 2 (LRRK2), Pten-Induced Kinase 1 (PINK1), Parkin(PRKN), and Protein deglycase (DJ-1) Are used in the transgenic models. An emerging model that combines both genetic- and neurotoxin-based methods has been generated to study the role of the immune system in the pathogenesis of PD. Here, we discuss the advantages and limitations of the different PD models and their utility for different research purposes.
Highlights
Parkinson’s disease (PD) is a chronic neurodegenerative disease named after James Parkinson who reported the clinical syndrome more than two centuries ago
Zebrafish displayed alteration in locomotor activity [23]. These findings suggest that the non-mammalian species are feasible model systems to study the molecular mechanism of the disease
Cellular models are ideal for large scale drug screening that could help narrow down potential drug targets for further validation in animal models [27]
Summary
Parkinson’s disease (PD) is a chronic neurodegenerative disease named after James Parkinson who reported the clinical syndrome more than two centuries ago. PD is the result of selective degeneration of dopaminergic neurons in the Substantia Nigra, which causes decreased level of dopamine in the striatum and lead to abnormal motor control [1]. The current treatment regime uses levodopa or dopaminergic agonists to target the primary pathophysiology of PD, which only alleviates the motor symptoms by restoring neurotransmission [4]. Long term use of these drugs can lead to severe side effects such as wearing-off symptoms and other motor complications [5,6]. The lack of access to human brains have led scientists to develop diverse range of experimental models using animals and in vitro cultured cells that could mimic different aspects of PD. Three major animal groups have been extensively used for modeling PD: rodents, non-human primates (NHP), and non-mammalian species. There are distinct advantages and limitations of each group which determine the suitability of the model for a specific experiment
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