ArticleExperimental neurology2018
α-synuclein expression from a single copy transgene increases sensitivity to stress and accelerates neuronal loss in genetic models of Parkinson's disease.
Article in Experimental neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Progress in modelling ATP13A2-linked neurodegeneration.NPJ Parkinson's disease · 2026Review
- Sorghum bicolor supplement attenuates rotenone-induced behavioral derangements in rats through neuroprotective mechanisms and modulation of tyrosine hydroxylase and α-synuclein/NF-kB immunopositive cells expressions.Journal of molecular histology · 2025Article
- Exploring Caenorhabditis elegans as Parkinson's Disease Model: Neurotoxins and Genetic Implications.Neurotoxicity research · 2024Review
- Animal models of Parkinson's disease: bridging the gap between disease hallmarks and research questions.Translational neurodegeneration · 2023Review
- ATP13A2 protects dopaminergic neurons in Parkinson's disease: from biology to pathology.Journal of biomedical research · 2022Article
- 1-Mesityl-3-(3-Sulfonatopropyl) Imidazolium Protects Against Oxidative Stress and Delays Proteotoxicity inFrontiers in pharmacology · 2022Article
- Functional Screening of Parkinson's Disease Susceptibility Genes to Identify Novel Modulators of α-Synuclein Neurotoxicity inFrontiers in aging neuroscience · 2022Article
- Review
- Modelling the functional genomics of Parkinson's disease in Caenorhabditis elegans: LRRK2 and beyond.Bioscience reports · 2021Review
- The Application of Nanotechnology for the Diagnosis and Treatment of Brain Diseases and Disorders.Frontiers in bioengineering and biotechnology · 2021Review
- Calpain mediated expansion of CD4+ cytotoxic T cells in rodent models of Parkinson's disease.Experimental neurology · 2020Article
- Dysregulated iron metabolism in C. elegans catp-6/ATP13A2 mutant impairs mitochondrial function.Neurobiology of disease · 2020Article
- Disruption of mitochondrial dynamics increases stress resistance through activation of multiple stress response pathways.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- Hepcidin-to-Ferritin Ratio Is Decreased in Astrocytes With Extracellular Alpha-Synuclein and Iron Exposure.Frontiers in cellular neuroscience · 2020Article
- Zn homeostasis in genetic models of Parkinson's disease in Caenorhabditis elegans.Journal of trace elements in medicine and biology : organ of the Society for Minerals and Trace Elements (GMS) · 2019Article
- Genetic Defects in Mitochondrial Dynamics inInternational journal of molecular sciences · 2019Article
- Found in Translation: The Utility ofBrain sciences · 2019Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Parkinson's disease (PD) is the second most common neurodegenerative disease and is characterized by the formation of α-synuclein-containing protein aggregates called Lewy bodies within the brain. A crucial role for α-synuclein in the pathogenesis of PD is also suggested by the fact that point mutations, increased copy number, or polymorphisms in the α-synuclein gene SNCA all cause or contribute to the development of PD. In addition to SNCA, an increasing number of other genes have been implicated in PD. While mutations in at least some of these genes have been shown to cause the formation of Lewy bodies, the role of α-synuclein in these genetic forms of PD remains poorly defined. Since C. elegans do not have a homolog of α-synuclein, this organism provides the opportunity to identify synergism between α-synuclein and other genes implicated in PD. To do this, we generated a novel C. elegans model in which wild-type α-synuclein is ubiquitously expressed from a single copy transgene, and examined the resulting effect on phenotypic deficits in PD deletion mutants affecting PARK2/pdr-1, PINK1/pink-1, DJ-1/djr-1.1 and ATP13A2/catp-6. While the PD deletion mutants exhibit only mild phenotypic deficits in absence of α-synuclein, expression of wild-type α-synuclein caused increased sensitivity to multiple stresses, induced deficits in dopamine-dependent behavior, and accelerated loss of dopamine neurons. Overall, these results suggest that the recessive loss of function mutations act together with α-synuclein to cause PD, and that α-synuclein lowering strategies may be effective in genetic forms of PD.
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