DYSTROPHIC NEURITES INFILTRATE EXTRACELLULAR NEUROFIBRILLARY TANGLES IN ALZHEIMER-DISEASE

被引:0
|
作者
VANDEWEGHE, J
CRAS, P
KAWAI, M
SIEDLAK, SL
TABATON, M
GREENBERG, B
PERRY, G
机构
[1] CASE WESTERN RESERVE UNIV,INST PATHOL,DIV NEUROPATHOL,2085 ADELBERT RD,CLEVELAND,OH 44106
[2] UNIV GENOA,INST NEUROL,I-16126 GENOA,ITALY
[3] UPJOHN CO,KALAMAZOO,MI 49001
关键词
ALZHEIMER DISEASE; AMYLOID; AMYLOID PRECURSOR PROTEIN; PAIRED HELICAL FILAMENT; SENILE PLAQUE; TAU;
D O I
暂无
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The neurotrophic activity of beta-amyloid protein (beta-AP) has been suggested to be responsible for the dystrophic neurites that surround beta-AP deposits in senile plaques of Alzheimer disease. The recent finding that neurofibrillary tangles (NFT) that remain as remnants in the extracellular space (E-NFT) after the death of the neuron contain beta-AP, suggested that dystrophic neurites might also be associated with E-NFT. In this study, we use a probe for E-NFT, basic fibroblast growth factor (bFGF)-binding to show that E-NFT do contain dystrophic neurites. Since these neurites contain the amyloid precursor protein whose cleavage can lead to beta-AP, they may also play a role in further beta-AP deposition in the E-NFT.
引用
收藏
页码:303 / 305
页数:3
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