ArticleBrain pathology (Zurich, Switzerland)2003
Neuropathology and neurodegeneration in rodent brain induced by lentiviral vector-mediated overexpression of alpha-synuclein.
Article in Brain pathology (Zurich, Switzerland), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed.
- An update on mammalian and non-mammalian animal models for biomarker development in neurodegenerative disorders.Cellular and molecular life sciences : CMLS · 2025Review
- Fiber deprivation and microbiome-borne curli shift gut bacterial populations and accelerate disease in a mouse model of Parkinson's disease.Cell reports · 2023Article
- Sequential or Simultaneous Injection of Preformed Fibrils and AAV Overexpression of Alpha-Synuclein Are Equipotent in Producing Relevant Pathology and Behavioral Deficits.Journal of Parkinson's disease · 2022Article
- The Small Molecule Alpha-Synuclein Aggregator, FN075, Enhances Alpha-Synuclein Pathology in Subclinical AAV Rat Models.Biomolecules · 2021Article
- Adeno-Associated Virus Expression of α-Synuclein as a Tool to Model Parkinson's Disease: Current Understanding and Knowledge Gaps.Aging and disease · 2021Review
- The Path to Progress Preclinical Studies of Age-Related Neurodegenerative Diseases: A Perspective on Rodent and hiPSC-Derived Models.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Review
- Reverse engineering Lewy bodies: how far have we come and how far can we go?Nature reviews. Neuroscience · 2021Review
- Polybrene induces neural degeneration by bidirectional CaCell death & disease · 2018Article
- The concept of alpha-synuclein as a prion-like protein: ten years after.Cell and tissue research · 2018Review
- Lentiviral vector-mediated overexpression of mutant ataxin-7 recapitulates SCA7 pathology and promotes accumulation of the FUS/TLS and MBNL1 RNA-binding proteins.Molecular neurodegeneration · 2016Article
- The contribution of alpha synuclein to neuronal survival and function - Implications for Parkinson's disease.Journal of neurochemistry · 2016Review
- Development of an Alpha-synuclein Based Rat Model for Parkinson's Disease via Stereotactic Injection of a Recombinant Adeno-associated Viral Vector.Journal of visualized experiments : JoVE · 2016Article
- Targeting α-synuclein oligomers by protein-fragment complementation for drug discovery in synucleinopathies.Expert opinion on therapeutic targets · 2015Article
- Definition of a molecular pathway mediating α-synuclein neurotoxicity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Evaluation of Models of Parkinson's Disease.Frontiers in neuroscience · 2015Review
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- Parkinson's disease: animal models and dopaminergic cell vulnerability.Frontiers in neuroanatomy · 2014Review
- rAAV2/7 vector-mediated overexpression of alpha-synuclein in mouse substantia nigra induces protein aggregation and progressive dose-dependent neurodegeneration.Molecular neurodegeneration · 2013Article
- Overexpression of mutant ataxin-3 in mouse cerebellum induces ataxia and cerebellar neuropathology.Cerebellum (London, England) · 2013Article
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6 authors.
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Abstract
Two mutations in alpha-synuclein, the main constituent of Lewy bodies, have been identified in familial Parkinson's disease. We have stereotactically injected lentiviral vectors encoding wild-type and A30P mutant human alpha-synuclein in different brain regions (striatum, substantia nigra, amygdala) of mice. Overexpression of alpha-synuclein induced time-dependent neuropathological changes reminiscent of Lewy pathology: abnormal accumulation of alpha-synuclein in cell bodies and neurites, alpha-synuclein-positive neuritic varicosities and cytoplasmic inclusions that stained with ubiquitin antibodies and became larger and more frequent with time. After one year, alpha-synuclein- and ubiquitin-positive neurons displayed a degenerative morphology and a significant loss of alpha-synuclein-positive cells was observed. Similar findings were observed with both the wild-type and the A30P mutant form of alpha-synuclein and this in different brain regions. This indicates that overexpression of alpha-synuclein is sufficient to induce Lewy-like pathology and neurodegeneration and that this effect is not restricted to dopaminergic cells. Our data also demonstrate the use of lentiviral vectors to create animal models for neurodegenerative diseases.
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