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The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

α-Synucleinopathy and selective dopaminergic neuron loss in a rat lentiviral-based model of Parkinson's disease

Lo Bianco, C., Ridet, J-L., Schneider, B. L., Déglon, N., Aebischer, P.·2002·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.152339799
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Abstract

Parkinson's disease (PD) is characterized by the progressive loss of substantia nigra dopaminergic neurons and the presence of cytoplasmic inclusions named Lewy bodies. Two missense mutations of the α-synuclein (α-syn; A30P and A53T) have been described in several families with an autosomal dominant form of PD. α-Syn also constitutes one of the main components of Lewy bodies in sporadic cases of PD. To develop an animal model of PD, lentiviral vectors expressing different human or rat forms of α-syn were injected into the substantia nigra of rats. In contrast to transgenic mice models, a selective loss of nigral dopaminergic neurons associated with a dopaminergic denervation of the striatum was observed in animals expressing either wild-type or mutant forms of human α-syn. This neuronal degeneration correlates with the appearance of abundant α-syn-positive inclusions and extensive neuritic pathology detected with both α-syn and silver staining. Lentiviral-mediated expression of wild-type or mutated forms of human α-syn recapitulates the essential neuropathological features of PD. Rat α-syn similarly leads to protein aggregation but without cell loss, suggesting that inclusions are not the primary cause of cell degeneration in PD. Viral-mediated genetic models may contribute to elucidate the mechanism of α-syn-induced cell death and allow the screening of candidate therapeutic molecules.

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  • Viral-mediated overexpression of wild-type or mutant SNCA in nigral neurons of rodents and non-human primates produces progressive motor dysfunction resembling Parkinson's disease motor symptoms.

    “Viral-mediated overexpression of wild-type or mutant SNCA within nigral neurons of rodents and non-human primates resulted in progressive motor dysfunction resembling the motor symptoms of PD patients [4–6].”

    From RNA binding protein AUF1/HNRNPD regulates nuclear export, stability and translation of SNCA transcripts (2023) · cites this paper as [5]

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Research works printed but not linked: 30

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Metadata

Authors
Lo Bianco, C., Ridet, J.-L., Schneider, B. L., Déglon, N., & Aebischer, P.
Affiliations
Institute of Neurosciences, Swiss Federal Institute of Technology Lausanne, EPFL, 1015 Lausanne, Switzerland; and Division of Surgical Research and Gene Therapy Center, Lausanne University Medical School, 1011 Lausanne, Switzerland
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2002-07-16
Volume
99
Issue
16
Pages
10813-10818
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.152339799
Cited by
482
References
4
Language
en

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