THE AMYLOID PRECURSOR PROTEIN IN ISCHEMIC BRAIN INJURY AND CHRONIC HYPOPERFUSION

被引:63
作者
KALARIA, RN
BHATTI, SU
LUST, WD
PERRY, G
机构
[1] CASE WESTERN RESERVE UNIV, DEPT NEUROL, CLEVELAND, OH 44106 USA
[2] CASE WESTERN RESERVE UNIV, DEPT NEUROSCI, CLEVELAND, OH 44106 USA
[3] CASE WESTERN RESERVE UNIV, DEPT NEUROL SURG, CLEVELAND, OH 44106 USA
[4] CASE WESTERN RESERVE UNIV, DEPT PATHOL, CLEVELAND, OH 44106 USA
来源
ALZHEIMERS DISEASE: AMYLOID PRECUSOR PROTEINS, SIGNAL TRANSDUCTION, AND NEURONAL TRANSPLANTATION | 1993年 / 695卷
关键词
D O I
10.1111/j.1749-6632.1993.tb23050.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
We studied changes in the spatial and temporal distribution of the beta amyloid precursor protein (APP) of Alzheimer's disease (AD) in experimental ischemic brain injury. Rats with repeated reversible occlusions of one middle cerebral artery showed striking APP reactivity in astrocytic processes in perifocal regions and adjacent white matter. APP reactive dystrophic axons and neurons were also evident in the cortex and hippocampus ipsilateral to the MCA occlusion. Such changes were similarly apparent in animals subjected to partial forebrain ischemia induced by bilateral occlusion of the carotid arteries. Our studies suggest that focal ischemic insults or chronic hypoperfusion leads to increased accumulation or induction of APP in surviving cellular elements that may relate to the processes involved in beta amyloid deposition in AD.
引用
收藏
页码:190 / 193
页数:4
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