Abstract
Parkinson’s disease (PD) ranks second among the most common neurodegenerative diseases, characterized by progressive and selective loss of dopaminergic neurons. Various cross-species preclinical models, including cellular models and animal models, have been established through the decades to study the etiology and mechanism of the disease from cell lines to nonhuman primates. These models are aimed at developing effective therapeutic strategies for the disease. None of the current models can replicate all major pathological and clinical phenotypes of PD. Selection of the model for PD largely relies on our interest of study. In this review, we systemically summarized experimental PD models, including cellular and animal models used in preclinical studies, to understand the pathogenesis of PD. This review is intended to provide current knowledge about the application of these different PD models, with focus on their strengths and limitations with respect to their contributions to the assessment of the molecular pathobiology of PD and identification of the therapeutic strategies for the disease.
Highlights
Parkinson's disease (PD) ranks second among the most common neurodegenerative diseases affecting millions of patients [1]
Selective loss of neurons in substantia nigra pars compacta (SNpc) constitutes nigrostriatal deficits observed in PD patients, such as tremor, rigidity, and akinesia, which can be substantially improved by treatment with dopamine modulators [2]
The advantages of cellular models over other models include the following: 1) they develop disease phenotypes more quickly; 2) they can more and reliably perform genetic or pharmacological manipulations and time-lapse imaging; 3) they require no ethical approval; and 4) they cost less. These properties of cellular models allow for large-scale testing within a short duration. Specific cell types such as dopaminergic neurons can be isolated for research, which facilitates the determination of PD pathogenesis
Summary
Parkinson's disease (PD) ranks second among the most common neurodegenerative diseases affecting millions of patients [1]. Various cross-species preclinical models, including cellular models and animal models, have been established through the decades to study the etiology and mechanism of the disease from cells to nonhuman primates (NHPs), including immortal cell lines, pluripotent stem cells (PSCs), nematodes (e.g., Caenorhabditis elegans), fruit flies, rodent animals, and NHPs (Fig.). Various cross-species preclinical models, including cellular models and animal models, have been established through the decades to study the etiology and mechanism of the disease from cells to nonhuman primates (NHPs), including immortal cell lines, pluripotent stem cells (PSCs), nematodes (e.g., Caenorhabditis elegans), fruit flies, rodent animals, and NHPs (Fig.1) These models are aimed at developing effective therapeutic strategies to slow or stop the progress of the disease. This review aims to provide current knowledge about the use of these different PD models, with focus on their strengths and limitations with respect to their contributions to the assessment of molecular pathobiology and identification of therapeutic strategies
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