Significance of intracellular Aβ42 accumulation in Alzheimer's disease

被引：54

作者：

Tabira, T

Chui, DH

Kuroda, S

机构：

[1] Natl Inst Longev Sci, Aichi 4748522, Japan

[2] Riken Brain Sci Inst, Lab Alzheimer Dis, Wako, Saitama 3510198, Japan

[3] Okayama Univ, Sch Med, Dept Neuropsychiat, Okayama 7008558, Japan

来源：

FRONTIERS IN BIOSCIENCE-LANDMARK | 2002年 / 7卷

关键词：

amyloid beta; apoptosis; presenilin; neurofibrillary tangle; senile plaque; cotton wool;

D O I：

10.2741/tabira

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：

Abeta plays a pivotal role in the pathogenesis of Alzheimer's disease (AD), but it is still obscure how it causes AD. We have established transgenic mice carrying wild-type or familial Alzheimer's disease (FAD) mutant-type presenilin 1 (PS1). In these mice, the number of cortical and hippocampal neurons decreased along with age in mutant mice. In addition, the old mutant mice showed a significant increase of dark neurons by silver staining and the number of neurons with intracellular Abeta42 by immunohistochemistry. Our extended study also showed a significant increase of intracellular Abeta42-positive neurons in isolated cases of AD as well as in PS1 mutant FAD cases. These neurons frequently showed apoptotic staining. However, coincidence of apoptotic markers and intraneuronal neurofibrillary tangles (NFT) was insignificant. Notably intraneuronal Abeta42-labeling was frequently seen in a case of AD showing cotton-wool type senile plaques with a few NFT positive neurons and dystrophic neurites. These results indicate that intraneuronal deposition of Abeta42 is important in the pathogenesis of AD.

引用

页码：A44 / A49

页数：6

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