Serum amyloid P is not present in amyloid β deposits of a transgenic animal model

被引:21
作者
Shi, J
Perry, G
Aliev, G
Smith, MA
Ashe, KH
Friedland, RP
机构
[1] Case Western Reserve Univ, Sch Med, Dept Neurol, Cleveland, OH 44106 USA
[2] Case Western Reserve Univ, Sch Med, Dept Pathol, Cleveland, OH 44106 USA
[3] Univ Minnesota, Dept Neurol, Minneapolis, MN 55455 USA
关键词
Alzheimer's disease; basic fibroblastic growth factor; blood-brain barrier; serum amyloid P component;
D O I
10.1097/00001756-199910190-00019
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
SERUM amyloid P component (SAP) is associated with amyloid beta (A beta) deposition in Alzheimer disease (AD). Since SAP is exclusively synthesized by peripheral organs, its presence in the brain of A beta suggests impairment of the blood-brain barrier (BBB). We studied the association of SAP with A beta deposits in a transgenic mouse model overexpressing beta-protein precursor (X PP). Both SAP and another extracellular matrix binding protein, basic fibroblastic growth factor bind to the heparinase sensitive sites of A beta deposits in this model. However, no endogenous SAP immunoreactivity was found in the transgenic mouse brain. These results suggest that SAP is not required for A beta deposition, and that this mouse model does not develop the same BBB abnormalities as those seen in AD. (C) 1999 Lippincott Williams & Wilkins.
引用
收藏
页码:3229 / 3232
页数:4
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