Cai Xiao-Dan. Golde Todd E. Younkin Steven G [a]. Release of excess amyloid beta protein from a mutant amyloid beta protein precursor, Science (Washington D C) 259(5094) :514-516, 1993.

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 wildtype 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.


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