α-internexin immunoreactivity reflects variable neuronal vulnerability in Alzheimer's disease and supports the role of the β-amyloid plaques in inducing neuronal injury

被引：38

作者：

Dickson, TC ^{[1
]}

Chuckowree, JA ^{[1
]}

Chuah, MI ^{[1
]}

West, AK ^{[1
]}

Vickers, JC ^{[1
]}

机构：

[1] Univ Tasmania, Discipline Pathol, NeuroRepair Grp, Hobart, Tas 7000, Australia

来源：

NEUROBIOLOGY OF DISEASE | 2005年 / 18卷 / 02期

基金：

英国医学研究理事会;

关键词：

Alzheimer's disease; neuronal trauma; neurofilament triplet proteins; alpha-internexin; neuronal injury; beta-amyloid plaque; tau; type IV intermediate filaments; neurodegeneration;

D O I：

10.1016/j.nbd.2004.10.001

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

This study investigated the role of alpha-internexin in the neuronal alterations associated with beta-amyloid plaque formation in Alzheimer's disease (AD). Cortical neurons could be defined by their variable content of neurofilament (NF) triplet and alpha-internexin proteins, with a distinct population of supragranular pyramidal cells containing alpha-internexin alone. Both NF triplet and alpha-internexin were localized to reactive axonal structures in physically damaged neurons in experimental trauma models. Similarly, NF triplet and alpha-internexin immunoreactive neurites were localized to plaques densely packed with beta-amyloid fibrils in preclinical AD cases, indicating that certain plaques may cause structural injury or impediment of local axonal transport. However, alpha-internexin, and not NF triplet, ring-like reactive neurites were present in end-stage AD cases, indicating the relatively late involvement of neurons that selectively contain alpha-internexin. These results implicate the expression of specific intermediate filament proteins in a distinct hierarchy of differential neuronal vulnerability to AD. (C) 2004 Elsevier Inc. All rights reserved.

引用

页码：286 / 295

页数：10

共 41 条

[21] Alterations in neurofilaments associated with reactive brain changes and axonal sprouting following acute physical injury to the rat neocortex [J].