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Animal Models of Parkinson’s Disease

Swanberg, Maria LU and Konnova, Elena A. (2018) p.83-106
Abstract
Parkinson’s disease (PD) is a heterogenous disease with a varying age of onset, symptoms, and rate of progression. This heterogeneity requires the use of a variety of animal models to study different aspects of the disease. Neurotoxin-based approaches include exposure of rodents or non-human primates to 6-OHDA, MPTP, and agrochemicals such as the pesticide rotenone, the herbicide paraquat, and the fungicide maneb. Acute exposure to neurotoxins induces motor deficits and rapid nigro-striatal dopaminergic cell death by disrupting mitochondrial function and/or increasing oxidative stress, while chronic administration of neurotoxins induces progressive models which can include alpha-synuclein (α-synuclein) aggregates. Genetic-based approaches... (More)
Parkinson’s disease (PD) is a heterogenous disease with a varying age of onset, symptoms, and rate of progression. This heterogeneity requires the use of a variety of animal models to study different aspects of the disease. Neurotoxin-based approaches include exposure of rodents or non-human primates to 6-OHDA, MPTP, and agrochemicals such as the pesticide rotenone, the herbicide paraquat, and the fungicide maneb. Acute exposure to neurotoxins induces motor deficits and rapid nigro-striatal dopaminergic cell death by disrupting mitochondrial function and/or increasing oxidative stress, while chronic administration of neurotoxins induces progressive models which can include alpha-synuclein (α-synuclein) aggregates. Genetic-based approaches to model Parkinson’s disease include transgenic models and viral vector-mediated models based on genes linked to monogenic Parkinson’s disease, including SNCA, LRRK2, UCH-L1, PRKN, PINK1, and and DJ-1, as well as manipulation of dopaminergic transcription factors. SNCA mutations, overexpression, and introduction of α-synuclein preformed fibrils induce toxic protein aggregates and variable nigro-striatal neurodegeneration and motor deficits, depending on the specific model. Species, genetic background of a strain, and environment affect the display of symptoms and neurodegenerative hallmarks of animal models. These models can be combined to study the interplay between genetics and environment and untangle the heterogeneity and mechanisms underlying Parkinson’s disease. In this chapter, we discuss the strengths and limitations of mouse, rat, and non-human primate models of Parkinson’s disease. (Less)
Please use this url to cite or link to this publication:
author
and
organization
publishing date
type
Chapter in Book/Report/Conference proceeding
publication status
published
subject
keywords
Parkinson's disease, Animal models, Rats, Mice, Transgenic mouse models, Transgene
host publication
Parkinson's Disease : Pathogenesis and Clinical Aspects - Pathogenesis and Clinical Aspects
editor
Stoker, Thomas B. and Greenland, Julia C.
pages
24 pages
publisher
Codon Publications
ISBN
978-0-9944381-6-4
DOI
10.15586/codonpublications.parkinsonsdisease.2018.ch5
language
English
LU publication?
yes
id
1ae2894d-75e3-4858-a4a6-ca0b7afcc1bc
date added to LUP
2019-06-19 10:22:10
date last changed
2020-06-09 11:52:05
@inbook{1ae2894d-75e3-4858-a4a6-ca0b7afcc1bc,
  abstract     = {{Parkinson’s disease (PD) is a heterogenous disease with a varying age of onset, symptoms, and rate of progression. This heterogeneity requires the use of a variety of animal models to study different aspects of the disease. Neurotoxin-based approaches include exposure of rodents or non-human primates to 6-OHDA, MPTP, and agrochemicals such as the pesticide rotenone, the herbicide paraquat, and the fungicide maneb. Acute exposure to neurotoxins induces motor deficits and rapid nigro-striatal dopaminergic cell death by disrupting mitochondrial function and/or increasing oxidative stress, while chronic administration of neurotoxins induces progressive models which can include alpha-synuclein (α-synuclein) aggregates. Genetic-based approaches to model Parkinson’s disease include transgenic models and viral vector-mediated models based on genes linked to monogenic Parkinson’s disease, including SNCA, LRRK2, UCH-L1, PRKN, PINK1, and and DJ-1, as well as manipulation of dopaminergic transcription factors. SNCA mutations, overexpression, and introduction of α-synuclein preformed fibrils induce toxic protein aggregates and variable nigro-striatal neurodegeneration and motor deficits, depending on the specific model. Species, genetic background of a strain, and environment affect the display of symptoms and neurodegenerative hallmarks of animal models. These models can be combined to study the interplay between genetics and environment and untangle the heterogeneity and mechanisms underlying Parkinson’s disease. In this chapter, we discuss the strengths and limitations of mouse, rat, and non-human primate models of Parkinson’s disease.}},
  author       = {{Swanberg, Maria and Konnova, Elena A.}},
  booktitle    = {{Parkinson's Disease : Pathogenesis and Clinical Aspects}},
  editor       = {{Stoker, Thomas B. and Greenland, Julia C.}},
  isbn         = {{978-0-9944381-6-4}},
  keywords     = {{Parkinson's disease; Animal models; Rats; Mice; Transgenic mouse models; Transgene}},
  language     = {{eng}},
  month        = {{12}},
  pages        = {{83--106}},
  publisher    = {{Codon Publications}},
  title        = {{Animal Models of Parkinson’s Disease}},
  url          = {{http://dx.doi.org/10.15586/codonpublications.parkinsonsdisease.2018.ch5}},
  doi          = {{10.15586/codonpublications.parkinsonsdisease.2018.ch5}},
  year         = {{2018}},
}