期刊
JOURNAL OF ALZHEIMERS DISEASE
卷 29, 期 4, 页码 875-881出版社
IOS PRESS
DOI: 10.3233/JAD-2012-120076
关键词
Aluminum; amyloid-beta; amyloid fibrils; copper; serum amyloid P component; transmission electron microscopy
资金
- EPSRC
- Keele Acorn Studentship
The mechanism whereby an under-saturated solution of amyloid-beta (A beta)(42) precipitates as beta sheets in vivo in Alzheimer's disease remains to be elucidated. Herein we present in vitro evidence that serum amyloid P component may mediate this process through its acceleration of amyloid formation from an under-saturated solution of A beta(42) and subsequently its stabilization of the amyloid fibrils formed over physiologically significant timeframes. Our observations support serum amyloid P component as a therapeutic target in Alzheimer's disease.
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