The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Age-Dependent Neurodegeneration and Alzheimer-Amyloid Plaque Formation in Transgenic Drosophila
Open accessAbstract
β-Amyloid peptides that are cleaved from the amyloid precursor protein (APP) play a critical role in Alzheimer's disease (AD) pathophysiology. Here, we show that in Drosophila, the targeted expression of the key genes of AD, APP, theβ-site APP-cleaving enzyme BACE, and the presenilins led to the generation of β-amyloid plaques and age-dependent neurodegeneration as well as to semilethality, a shortened life span, and defects in wing vein development. Genetic manipulations or pharmacological treatments with secretase inhibitors influenced the activity of the APP-processing proteases and modulated the severity of the phenotypes. This invertebrate model of amyloid plaque pathology demonstrates Aβ-induced neurodegeneration as a basic biological principle and may allow additional genetic analyses of the underlying molecular pathways.
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Cites
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
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The Genome Sequence of Drosophila melanogaster
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“…accumulation and deposition of -amyloid (A) peptides in senile plaques, by the formation of neurofibrillary tangles (NFT) composed of abnormally phosphorylated forms of the microtubule binding protein tau, and by a progressive neuronal damage and cell loss (Gomez-Isla et al., 1996; Selkoe, 1999).”
BackgroundPurification and cloning of amyloid precursor protein β-secretase from human brain
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Cited by
Drosophila as a Model for Human Neurodegenerative Disease
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Efficient Inhibition of the Alzheimer's Disease β-Secretase by Membrane Targeting
Rajendran, L., Schneider, A., Schlechtingen, G., Weidlich, S., Ries, J., Braxmeier, T., Schwille, P., Schulz, J. B., Schroeder, C., Simons, M., et al. (2008) · Science · doi:10.1126/science.1156609 · Cited by 262
Muhammad, A., Flores, I., Zhang, H., Yu, R., Staniszewski, A., Planel, E., Herman, M., Ho, L., Kreber, R., Honig, L. S., et al. (2008) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0802545105 · Cited by 248
Drosophila melanogaster as a model organism for Alzheimer’s disease
Prüßing, K., Voigt, A., & Schulz, J. B. (2013) · Molecular Neurodegeneration · doi:10.1186/1750-1326-8-35 · Cited by 235
Metadata
- Authors
- Greeve, I., Kretzschmar, D., Tschäpe, J.-A., Beyn, A., Brellinger, C., Schweizer, M., Nitsch, R. M., & Reifegerste, R.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2004-04-21
- Volume
- 24
- Issue
- 16
- Pages
- 3899-3906
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W2163240161
- Cited by
- 287
- References
- 42
- FWCI
- 7.60
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Greeve, I., Kretzschmar, D., Tschäpe, J.-A., Beyn, A., Brellinger, C., Schweizer, M., Nitsch, R. M., & Reifegerste, R. (2004). Age-Dependent Neurodegeneration and Alzheimer-Amyloid Plaque Formation in Transgenic Drosophila. The Journal of Neuroscience. https://doi.org/10.1523/jneurosci.0283-04.2004
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.