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From iPS Cells to Rodents and Nonhuman Primates : Filling Gaps in Modeling Parkinson's Disease

Outeiro, Tiago F. ; Heutink, Peter ; Bezard, Erwan and Cenci, Angela M. LU orcid (2021) In Movement Disorders 36(4). p.832-841
Abstract

Parkinson's disease (PD) is primarily known as a movement disorder because of typical clinical manifestations associated with the loss of dopaminergic neurons in the substantia nigra. However, it is now widely recognized that PD is a much more complex condition, with multiple and severe nonmotor features implicating additional brain areas and organs in the disease process. Pathologically, typical forms of PD are characterized by the accumulation of α-synuclein-rich protein inclusions known as Lewy bodies and Lewy neurites, although other types of protein inclusions are also often present in the brain. Familial forms of PD have provided a wealth of information about molecular pathways leading to neurodegeneration, but only to add to the... (More)

Parkinson's disease (PD) is primarily known as a movement disorder because of typical clinical manifestations associated with the loss of dopaminergic neurons in the substantia nigra. However, it is now widely recognized that PD is a much more complex condition, with multiple and severe nonmotor features implicating additional brain areas and organs in the disease process. Pathologically, typical forms of PD are characterized by the accumulation of α-synuclein-rich protein inclusions known as Lewy bodies and Lewy neurites, although other types of protein inclusions are also often present in the brain. Familial forms of PD have provided a wealth of information about molecular pathways leading to neurodegeneration, but only to add to the complexity of the problem and uncover new knowledge gaps. Therefore, modeling PD in the laboratory has become increasingly challenging. Here, we discuss knowledge gaps and challenges in the use of laboratory models for the study of a disease that is clinically heterogeneous and multifactorial. We propose that the combined use of patient-derived cells and animal models, along with current technological tools, will not only expand our molecular and pathophysiological understanding of PD, but also assist in the identification of therapeutic strategies targeting relevant pathogenic pathways.

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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
animal models, iPS cells, neurodegeneration, pathophysiology, α-synuclein
in
Movement Disorders
volume
36
issue
4
pages
10 pages
publisher
John Wiley & Sons Inc.
external identifiers
  • pmid:33200446
  • scopus:85096665907
ISSN
0885-3185
DOI
10.1002/mds.28387
language
English
LU publication?
yes
id
b25ee308-7482-46af-9cf7-012718e61823
date added to LUP
2020-12-09 08:23:15
date last changed
2022-06-14 08:14:05
@article{b25ee308-7482-46af-9cf7-012718e61823,
  abstract     = {{<p>Parkinson's disease (PD) is primarily known as a movement disorder because of typical clinical manifestations associated with the loss of dopaminergic neurons in the substantia nigra. However, it is now widely recognized that PD is a much more complex condition, with multiple and severe nonmotor features implicating additional brain areas and organs in the disease process. Pathologically, typical forms of PD are characterized by the accumulation of α-synuclein-rich protein inclusions known as Lewy bodies and Lewy neurites, although other types of protein inclusions are also often present in the brain. Familial forms of PD have provided a wealth of information about molecular pathways leading to neurodegeneration, but only to add to the complexity of the problem and uncover new knowledge gaps. Therefore, modeling PD in the laboratory has become increasingly challenging. Here, we discuss knowledge gaps and challenges in the use of laboratory models for the study of a disease that is clinically heterogeneous and multifactorial. We propose that the combined use of patient-derived cells and animal models, along with current technological tools, will not only expand our molecular and pathophysiological understanding of PD, but also assist in the identification of therapeutic strategies targeting relevant pathogenic pathways.</p>}},
  author       = {{Outeiro, Tiago F. and Heutink, Peter and Bezard, Erwan and Cenci, Angela M.}},
  issn         = {{0885-3185}},
  keywords     = {{animal models; iPS cells; neurodegeneration; pathophysiology; α-synuclein}},
  language     = {{eng}},
  month        = {{04}},
  number       = {{4}},
  pages        = {{832--841}},
  publisher    = {{John Wiley & Sons Inc.}},
  series       = {{Movement Disorders}},
  title        = {{From iPS Cells to Rodents and Nonhuman Primates : Filling Gaps in Modeling Parkinson's Disease}},
  url          = {{http://dx.doi.org/10.1002/mds.28387}},
  doi          = {{10.1002/mds.28387}},
  volume       = {{36}},
  year         = {{2021}},
}