Release of excess amyloid beta protein from a mutant amyloid beta protein precursor
- PMID: 8424174
- DOI: 10.1126/science.8424174
Release of excess amyloid beta protein from a mutant amyloid beta protein precursor
Abstract
The 4-kilodalton amyloid beta protein (A beta), which forms fibrillar deposits in Alzheimer's disease (AD), is derived from a large protein referred to as the amyloid beta protein precursor (beta APP). Human neuroblastoma (M17) cells transfected with constructs expressing wild-type beta APP or a mutant, beta APP delta NL, recently linked to familial AD were compared. After continuous metabolic labeling for 8 hours, cells expressing beta APP delta NL had five times more of an A beta-bearing, carboxyl terminal, beta APP derivative than cells expressing wild-type beta APP and they released six times more A beta into the medium. Thus this mutant beta APP may cause AD because its processing is altered in a way that releases increased amounts of A beta.
Comment in
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Alzheimer's pathology begins to yield its secrets.Science. 1993 Jan 22;259(5094):457-8. doi: 10.1126/science.8424167. Science. 1993. PMID: 8424167 No abstract available.
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