Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1 View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1996-10

AUTHORS

K Duff, C Eckman, C Zehr, X Yu, C M Prada, J Perez-tur, M Hutton, L Buee, Y Harigaya, D Yager, D Morgan, M N Gordon, L Holcomb, L Refolo, B Zenk, J Hardy, S Younkin

ABSTRACT

Mutations in the genes encoding amyloid-beta precursor protein (APP), presenilin 1 (PS1) and presenilin 2 (PS2) are known to cause early-onset, autosomal dominant Alzheimer's disease. Studies of plasma and fibroblasts from subjects with these mutations have established that they all alter amyloid beta-protein (beta APP) processing, which normally leads to the secretion of amyloid-beta protein (relative molecular mass 4,000; M(r) 4K; approximately 90% A beta1-40, approximately 10% A beta1-42(43)), so that the extracellular concentration of A beta42(43) is increased. This increase in A beta42(43) is believed to be the critical change that initiates Alzheimer's disease pathogenesis because A beta42(43) is deposited early and selectively in the senile plaques that are observed in the brains of patients with all forms of the disease. To establish that the presenilin mutations increase the amount of A beta42(43) in the brain and to test whether presenilin mutations act as true (gain of function) dominants, we have now constructed mice expressing wild-type and mutant presenilin genes. Analysis of these mice showed that overexpression of mutant, but not wild-type, PS1 selectively increases brain A beta42(43). These results indicate that the presenilin mutations probably cause Alzheimer's disease through a gain of deleterious function that increases the amount of A beta42(43) in the brain. More... »

PAGES

710-713

Journal

TITLE

Nature

ISSUE

6602

VOLUME

383

Author Affiliations

From Grant

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/383710a0

    DOI

    http://dx.doi.org/10.1038/383710a0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1044462663

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/8878479


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