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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