A Drosophila model of Parkinson's disease

By M. Feany, W. Bender. Nature, 2000

2,108 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/defd337b07876fb80bee56e80c78e2f1e32412a1

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In Cellular and Molecular Neuroscience

In Neurology

In Physiology

Citations in the corpus

The Fly as a Model for Neurodegenerative Diseases: Is It Worth the Jump? (2007, positive): “reported that flies treated with rotenone, which is a mitochondrial complex I inhibitor and a widely used pesticide, recapitulated the main symptomatic features of PD including locomotor impairments and loss of dopaminergic neurons in all of the brain clusters. The antioxidant melatonin alleviated b”
The art and design of genetic screens: Drosophila melanogaster (2002, neutral): “Furthermore, 197 out of 287 known human disease genes have Drosophila homologues, and even those that do not can produce very similar symptoms when expressed in flie”
Α-synuclein misfolding and Parkinson's disease. (2012, background): “Here, a substantial portion of total protein in these inclusions is composed of α-synuclein [4, 10]; • The production of wild type α-synuclein in transgenic mice [11] or expression of WT, A30P, or A53T α-synuclein in transgenic flies [12]”
A Role for α-Synuclein in the Regulation of Dopamine Biosynthesis (2002, background): “-Synuclein inclusions occur in several animal models (Betarbet et al., 2000; Feany and Bender, 2000; Kowall et al., 2000; Masliah et al., 2000), and cell-free studies confirm that”
Alpha-synuclein, especially the Parkinson's disease-associated mutants, forms pore-like annular and tubular protofibrils. (2002, background): “Third, transgenic mice and Drosophila expressing human wild-type (WT) a-synuclein or, in the flies, the mutants, are characterized by a-synuclein inclusions that resemble Lewy bodies.(7,8) In both models, the formation of these inclusions is correlated to the onset of disease phenotype.”
Targeted gene expression in Drosophila dopaminergic cells using regulatory sequences from tyrosine hydroxylase. (2003, methodology): “We quantified this behavior by adapting a startle-induced wall climbing assay that was previously used to monitor locomotion defects (Ganetzky and Flanagan, 1978; Bainton et al., 2000; Feany and Bender, 2000 ).”
Drosophila, the golden bug, emerges as a tool for human genetics (2005, background): “Although flies do not have an obvious homologue of SNCA , misexpression of the mutant but not normal forms of the human protein results in late-onset neurodegeneration in the fly ey”
Animal models of Parkinson's disease: a source of novel treatments and clues to the cause of the disease (2011, background): “Feany and Bender (2000) first reported production of the a-synuclein transgenic Drosophila model of PD.”