The DOI matches its Crossref record; 41 of the 41 references it cites were found in a registry or an index.
Amyloid-β Aggregation
Abstract
Alzheimer’s disease (AD) is the most prevalent neurodegenerative disease in the growing population of elderly people. A hallmark of AD is the accumulation of plaques in the brain of AD patients. The plaques predominantly consist of aggregates of amyloid-β (Aβ), a peptide of 39–42 amino acids generated in vivo by specific, proteolytic cleavage of the amyloid precursor protein. There is a growing body of evidence that Aβ aggregates are ordered oligomers and the cause rather than a product of AD. The analysis of the assembly pathway of Aβ in vitro and biochemical characterization of Aβ deposits isolated from AD brains indicate that Aβ oligomerization occurs via distinct intermediates, including oligomers of 3–50 Aβ monomers, annular oligomers, protofibrils, fibrils and plaques. Of these, the most toxic species appear to be small Aβ oligomers. This article reviews the current knowledge of the mechanism of Aβ assembly in vivo and in vitro, as well as the influence of inherited amino acid replacements in Aβ and experimental conditions on Aβ aggregation. Challenges regarding the reproducible handling of the Aβ peptide for in vitro assembly studies are discussed.
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1 retracted
RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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The precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor
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Cited by
Amyloid β-Protein Assembly and Alzheimer Disease
Roychaudhuri, R., Yang, M., Hoshi, M. M., & Teplow, D. B. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.r800036200 · Cited by 615
Mechanism of amyloid plaque formation suggests an intracellular basis of Aβ pathogenicity
Friedrich, R. P., Tepper, K., Rönicke, R., Soom, M., Westermann, M., Reymann, K., Kaether, C., & Fändrich, M. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0904532106 · Cited by 303
Recent advances in our understanding of neurodegeneration
Jellinger, K. A. (2009) · Journal of Neural Transmission · doi:10.1007/s00702-009-0240-y · Cited by 274
Baik, S. H., Kang, S., Son, S. M., & Mook-Jung, I. (2016) · Glia · doi:10.1002/glia.23074 · Cited by 234
Broersen, K., Rousseau, F., & Schymkowitz, J. (2010) · Alzheimer's Research & Therapy · doi:10.1186/alzrt36 · Cited by 168
Metadata
- Authors
- Finder, V. H., & Glockshuber, R.
- Venue
- Neurodegenerative Diseases
- Publisher
- S. Karger AG
- Published
- 2007
- Volume
- 4
- Issue
- 1
- Pages
- 13-27
- ISSN
- 1660-2854 (ISSN-L)
- 1660-2862
- OpenAlex
- W2027250745
- Cited by
- 348
- References
- 41
- FWCI
- 10.68
- Type
- journal article
- Language
- en
- Open access
- closed
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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.