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Viral vector-mediated overexpression of α-synuclein as a progressive model of Parkinson's disease

Ulusoy, Ayse LU ; Decressac, Mickael LU ; Kirik, Deniz LU and Björklund, Anders LU orcid (2010) In Progress in Brain Research 184. p.89-111
Abstract

The discovery of the role of α-synuclein in the pathogenesis of Parkinson's disease (PD) has opened new possibilities for the development of more authentic models of Parkinson's disease. Recombinant adeno-associated virus (AAV) and lentivirus (LV) vectors are efficient tools for expression of genes locally in subsets of neurons in the brain and can be used to express human wild-type or mutated α-synuclein selectively in midbrain dopamine neurons. Using this approach, it is possible to trigger extensive PD-like cellular and axonal pathologies in the nigrostriatal projection, involving abnormal protein aggregation, neuronal dysfunction, and cell death that develop progressively over time. Targeted overexpression of human α-synuclein in... (More)

The discovery of the role of α-synuclein in the pathogenesis of Parkinson's disease (PD) has opened new possibilities for the development of more authentic models of Parkinson's disease. Recombinant adeno-associated virus (AAV) and lentivirus (LV) vectors are efficient tools for expression of genes locally in subsets of neurons in the brain and can be used to express human wild-type or mutated α-synuclein selectively in midbrain dopamine neurons. Using this approach, it is possible to trigger extensive PD-like cellular and axonal pathologies in the nigrostriatal projection, involving abnormal protein aggregation, neuronal dysfunction, and cell death that develop progressively over time. Targeted overexpression of human α-synuclein in midbrain dopamine neurons, using AAV vectors, reproduces many of the characteristic features of the human disease and provides, for the first time, a model of progressive PD that can be applied to both rodents and primates.

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author
; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Synuclein, Dopamine, Nigrostriatal system, Motor impairment, Adeno-associated virus, Lentivirus, Viral vectors, Animal models
in
Progress in Brain Research
volume
184
pages
23 pages
publisher
Elsevier
external identifiers
  • wos:000287856300006
  • scopus:77957224859
  • pmid:20887871
ISSN
1875-7855
DOI
10.1016/S0079-6123(10)84005-1
language
English
LU publication?
yes
id
084e1107-2d8f-4fce-bb2d-3425f6845593 (old id 1859368)
date added to LUP
2016-04-01 14:31:51
date last changed
2022-04-14 18:17:34
@article{084e1107-2d8f-4fce-bb2d-3425f6845593,
  abstract     = {{<p>The discovery of the role of α-synuclein in the pathogenesis of Parkinson's disease (PD) has opened new possibilities for the development of more authentic models of Parkinson's disease. Recombinant adeno-associated virus (AAV) and lentivirus (LV) vectors are efficient tools for expression of genes locally in subsets of neurons in the brain and can be used to express human wild-type or mutated α-synuclein selectively in midbrain dopamine neurons. Using this approach, it is possible to trigger extensive PD-like cellular and axonal pathologies in the nigrostriatal projection, involving abnormal protein aggregation, neuronal dysfunction, and cell death that develop progressively over time. Targeted overexpression of human α-synuclein in midbrain dopamine neurons, using AAV vectors, reproduces many of the characteristic features of the human disease and provides, for the first time, a model of progressive PD that can be applied to both rodents and primates.</p>}},
  author       = {{Ulusoy, Ayse and Decressac, Mickael and Kirik, Deniz and Björklund, Anders}},
  issn         = {{1875-7855}},
  keywords     = {{Synuclein; Dopamine; Nigrostriatal system; Motor impairment; Adeno-associated virus; Lentivirus; Viral vectors; Animal models}},
  language     = {{eng}},
  pages        = {{89--111}},
  publisher    = {{Elsevier}},
  series       = {{Progress in Brain Research}},
  title        = {{Viral vector-mediated overexpression of α-synuclein as a progressive model of Parkinson's disease}},
  url          = {{http://dx.doi.org/10.1016/S0079-6123(10)84005-1}},
  doi          = {{10.1016/S0079-6123(10)84005-1}},
  volume       = {{184}},
  year         = {{2010}},
}