Release of excess amyloid β protein from a mutant amyloid β protein precursor

Xiao Dan Cai, Todd E. Golde, Steven G. Younkin

Research output: Contribution to journalArticlepeer-review

797 Scopus citations


The 4-kilodalton amyloid β protein (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, βAPPσNL, recently linked to familial AD were compared. After continuous metabolic labeling for 8 hours, cells expressing βAPPΔNL 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.

Original languageEnglish (US)
Pages (from-to)514-516
Number of pages3
Issue number5094
StatePublished - Jan 22 1993

ASJC Scopus subject areas

  • General


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