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Science 12 January 1996:
Vol. 271. no. 5246, p. 159
DOI: 10.1126/science.271.5246.159
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Perspectives

Nazneen N. Dewji, S. Jonathan Singer

All cases of familial Alzheimer's disease are caused by mutations in either the gene for beta-amyloid precursor protein or the protein S182/STM. The normal functions of these transmembrane proteins are unknown, and it is unclear how they relate to one another. N. N. Dewji and S. J. Singer propose that these two proteins interact in a way analogous to the Sevenless and Bride of Sevenless proteins in the developing Drosophila eye and the lin-12 and sel-12 proteins in the developing vulva of Caenorhabditis elegans. He suggests that excess deposition of amyloid, a hallmark and likely cause of Alzheimer's disease, would be a result of the abnormal processing of the protein-protein complex.

This proposal is likely to provoke responses from the community. If you have a question or would like to comment on the ideas presented by Drs. Dewji and Singer in this Perspective or if you would like to read the comments posted by others, please go to our interactive Forum (click on the Forum button below). You can also read the full text of this Perspective by clicking on the Full Text button below.

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The authors are in the Department of Biology, University of California, San Diego, La Jolla, CA 92093, USA.


THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES:
An early specific cell-cell interaction occurs in the production of beta-amyloid in cell cultures.
N. N. Dewji, D. Mukhopadhyay, and S. J. Singer (2006)
PNAS 103, 1540-1545
   Abstract »    Full Text »    PDF »
Single Transmembrane Spanning Heterotrimeric G Protein-Coupled Receptors and Their Signaling Cascades.
T. B. Patel (2004)
Pharmacol. Rev. 56, 371-385
   Abstract »    Full Text »    PDF »
Risk Factors for Alzheimer's Disease: Role of Multiple Antioxidants, Non-Steroidal Anti-inflammatory and Cholinergic Agents Alone or in Combination in Prevention and Treatment.
K. N. Prasad, W. C. Cole, and K. C. Prasad (2002)
J. Am. Coll. Nutr. 21, 506-522
   Abstract »    Full Text »    PDF »
Specific intercellular binding of the beta -amyloid precursor protein to the presenilins induces intercellular signaling: Its significance for Alzheimer's disease.
N. N. Dewji and S. J. Singer (1998)
PNAS 95, 15055-15060
   Abstract »    Full Text »    PDF »
Additional evidence for an eight-transmembrane-domain topology for Caenorhabditis elegans and human presenilins.
X. Li and I. Greenwald (1998)
PNAS 95, 7109-7114
   Abstract »    Full Text »    PDF »
The seven-transmembrane spanning topography of the Alzheimer disease-related presenilin proteins in the plasma membranes of cultured cells.
N. N. Dewji and S. J. Singer (1997)
PNAS 94, 14025-14030
   Abstract »    Full Text »    PDF »
On the spurious endoproteolytic processing of the presenilin proteins in cultured cells and tissues.
N. N. Dewji, C. Do, and S. J. Singer (1997)
PNAS 94, 14031-14036
   Abstract »    Full Text »    PDF »
Cell surface expression of the Alzheimer disease-related presenilin proteins.
N. N. Dewji and S. J. Singer (1997)
PNAS 94, 9926-9931
   Abstract »    Full Text »    PDF »


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Science. ISSN 0036-8075 (print), 1095-9203 (online)