作者: Matthew Mold , Annette K Shrive , Christopher Exley , None
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摘要: The mechanism whereby an under-saturated solution of amyloid-β (Aβ)42 precipitates as β sheets in vivo Alzheimer's disease remains to be elucidated. Herein we present vitro evidence that serum amyloid P component may mediate this process through its acceleration formation from Aβ42 and subsequently stabilization the fibrils formed over physiologically significant timeframes. Our observations support a therapeutic target disease.