Abstract
The 4-kilodalton amyloid βprotein (Aβ), which forms fibrillar deposits in Alzheimer's disease (AD), is derived from a large protein referred to as the amyloid β protein precursor (βAPP). Human neuroblastoma (M17) cells transfected with constructs expressing wild-type βAPP or a mutant, βAPP ΔNL , recently linked to familial AD were compared. After continuous metabolic labeling for 8 hours, cells expressing β APP ΔNL had five times more of an Aβ-bearing, carboxyl terminal, βAPP derivative than cells expressing wild-type βAPP and they released six times more Aβ into the medium. Thus this mutant βAPP may cause AD because its processing is altered in a way that releases increased amounts of Aβ.
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Dates
Type | When |
---|---|
Created | 18 years, 10 months ago (Oct. 5, 2006, 7:05 p.m.) |
Deposited | 1 year, 7 months ago (Jan. 15, 2024, 5:20 a.m.) |
Indexed | 1 day, 22 hours ago (Aug. 30, 2025, 1:07 p.m.) |
Issued | 32 years, 7 months ago (Jan. 22, 1993) |
Published | 32 years, 7 months ago (Jan. 22, 1993) |
Published Print | 32 years, 7 months ago (Jan. 22, 1993) |
@article{Cai_1993, title={Release of Excess Amyloid β Protein from a Mutant Amyloid β Protein Precursor}, volume={259}, ISSN={1095-9203}, url={http://dx.doi.org/10.1126/science.8424174}, DOI={10.1126/science.8424174}, number={5094}, journal={Science}, publisher={American Association for the Advancement of Science (AAAS)}, author={Cai, Xiao-Dan and Golde, Todd E. and Younkin, Steven G.}, year={1993}, month=jan, pages={514–516} }