The DOI matches its Crossref record; 13 of the 13 references it cites were found in a registry or an index.
Dissecting the pathological effects of human Aβ40 and Aβ42 in Drosophila : A potential model for Alzheimer's disease
Abstract
Accumulation of amyloid-β (Aβ) peptides in the brain has been suggested to be the primary event in sequential progression of Alzheimer's disease (AD). Here, we use Drosophila to examine whether expression of either the human Aβ40 or Aβ42 peptide in the Drosophila brain can induce pathological phenotypes resembling AD. The expression of Aβ42 led to the formation of diffused amyloid deposits, age-dependent learning defects, and extensive neurodegeneration. In contrast, expression of Aβ40 caused only age-dependent learning defects but did not lead to the formation of amyloid deposits or neurodegeneration. These results strongly suggest that accumulation of Aβ42 in the brain is sufficient to cause behavioral deficits and neurodegeneration. Moreover, Drosophila may serve as a model for facilitating the understanding of molecular mechanisms underlying Aβ toxicity and the discovery of novel therapeutic targets for AD.
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“The fly model of AD displays many features of the disease, including Ab deposition in the brain, neuronal degeneration, locomotor dysfunction, and memory deficits (37)(38)(39).”
From Differential protective effects of connective tissue growth factor against Aβ neurotoxicity on neurons and glia (2017) · cites this paper as [38]
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“Significantly, such Aβ42 accumulation was associated with neurodegeneration.”
From Aβ42 Is Essential for Parenchymal and Vascular Amyloid Deposition in Mice (2005) · cites this paper as Iijima et al., 2004
In the citing paper
“Expression of Aβ1-42, but not Aβ1-40, promoted peptide accumulation of diffuse intracellular and extracellular deposits in the transgenic flies.”
From Aβ42 Is Essential for Parenchymal and Vascular Amyloid Deposition in Mice (2005) · cites this paper as Iijima et al., 2004
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Alternatives to animal testing: a review
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Aβ42 Is Essential for Parenchymal and Vascular Amyloid Deposition in Mice
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Metadata
- Authors
- Iijima, K., Liu, H.-P., Chiang, A.-S., Hearn, S. A., Konsolaki, M., & Zhong, Y.
- Affiliations
- Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, NY 11724; Department of Life Science, National Tsing Hua University, Hsinchu 30043, Taiwan; and Department of Functional Genomics, Novartis Institute for Biomedical Research, Novartis Pharmaceuticals, 556 Morris Avenue, Summit, NJ 07901
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2004-04-06
- Volume
- 101
- Issue
- 17
- Pages
- 6623-6628
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 440
- References
- 13
- Language
- en
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