The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.
Evidence that β-Amyloid Protein in Alzheimer's Disease Is Not Derived by Normal Processing
Abstract
The β-amyloid protein (β/A4), derived from a larger amyloid precursor protein (APP), is the principal component of senile plaques in Alzheimer's disease. APP is an integral membrane glycoprotein and is secreted as a carboxyl-terminal truncated molecule. APP cleavage, which is a membrane-associated event, occurred at a site located within the β/A4 region. This suggests that an intact amyloidogenic β/A4 fragment is not generated during normal APP catabolism. Therefore, an early event in amyloid formation may involve altered APP processing that results in the release and subsequent deposition of intact β/A4.
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Citations
Cites
The precursor of Alzheimer's disease amyloid A4 protein resembles a cell-surface receptor
Kang, J., Lemaire, H.-G., Unterbeck, A., Salbaum, J. M., Masters, C. L., Grzeschik, K.-H., Multhaup, G., Beyreuther, K., & Müller-Hill, B. (1987) · Nature · doi:10.1038/325733a0 · Cited by 4,619
Self-citationBlessed, G., Tomlinson, B. E., & Roth, M. (1968) · British Journal of Psychiatry · doi:10.1192/bjp.114.512.797 · Cited by 4,117
Cited by
Alzheimer's disease: the amyloid cascade hypothesis
Hardy, J. A., & Higgins, G. A. (1992) · Science · doi:10.1126/science.1566067 · Cited by 7,484
Alzheimer's Disease: Genes, Proteins, and Therapy
Selkoe, D. J. (2001) · Physiological Reviews · doi:10.1152/physrev.2001.81.2.741 · Cited by 6,063
Amyloid β-peptide is produced by cultured cells during normal metabolism
Haass, C., Schlossmacher, M. G., Hung, A. Y., Vigo-Pelfrey, C., Mellon, A., Ostaszewski, B. L., Lieberburg, I., Koo, E. H., Schenk, D., Teplow, D. B., et al. (1992) · Nature · doi:10.1038/359322a0 · Cited by 1,921
Self-citationCitron, M., Oltersdorf, T., Haass, C., McConlogue, L., Hung, A. Y., Seubert, P., Vigo-Pelfrey, C., Lieberburg, I., & Selkoe, D. J. (1992) · Nature · doi:10.1038/360672a0 · Cited by 1,757
Production of the Alzheimer Amyloid β Protein by Normal Proteolytic Processing
Shoji, M., Golde, T. E., Ghiso, J., Cheung, T. T., Estus, S., Shaffer, L. M., Cai, X.-D., McKay, D. M., Tintner, R., Frangione, B., et al. (1992) · Science · doi:10.1126/science.1439760 · Cited by 1,447
Metadata
- Authors
- Sisodia, S. S., Koo, E. H., Beyreuther, K., Unterbeck, A., & Price, D. L.
- Venue
- Science
- Published
- 1990-04-27
- Volume
- 248
- Issue
- 4954
- Pages
- 492-495
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2071691905
- Cited by
- 893
- References
- 2
- FWCI
- 62.36
- Type
- journal article
- Language
- en
- Open access
- closed
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- CoChat. (2026). Citation check: Evidence that β-Amyloid Protein in Alzheimer's Disease Is Not Derived by Normal Processing. https://app.cochat.ai/papers/10.1126/science.1691865
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- Sisodia, S. S., Koo, E. H., Beyreuther, K., Unterbeck, A., & Price, D. L. (1990). Evidence that β-Amyloid Protein in Alzheimer's Disease Is Not Derived by Normal Processing. Science. https://doi.org/10.1126/science.1691865
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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.
