β-amyloid deposition and neurofibrillary tangle association with caspase activation in Down syndrome

被引：19

作者：

Head, E ^{[1
]}

Lott, IT

Cribbs, DH

Cotman, CW

Rohn, TT

机构：

[1] Univ Calif Irvine, Gillespie Neurosci Res Facil 1529, Inst Brain Aging & Dementia, Irvine, CA 92697 USA

[2] Univ Calif Irvine, Mental Retardat Ctr, Dept Pediat, Irvine, CA 92697 USA

[3] Boise State Univ, Dept Biol, Boise, ID 83725 USA

来源：

NEUROSCIENCE LETTERS | 2002年 / 330卷 / 01期

关键词：

Down syndrome; apoptosis; caspase-8; caspase-3; beta-amyloid; neurofibrillary tangles;

D O I：

10.1016/S0304-3940(02)00705-X

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Individuals with Down syndrome (DS) and Alzheimer's disease (AD) develop senile plaques, neurofibrillary tangles (NFT), and neuron loss. Recent studies demonstrate the activation of apoptotic pathways in AD; less data is available in DS. The DS brain was examined using immunocytochemistry and antibodies against the active fragment of caspase-8 (AC, 8) and to caspase-3 cleavage products of fodrin (CCP), a neuronal cytoskeleton protein. The hippocampus demonstrated widespread accumulation of fodrin CCP and AC8 in NFTs and dystrophic neurites. Individual neurons contained intracellular beta-amyloid (Abeta) and fodrin CCP providing evidence that caspase activation can occur with both NFT and Abeta. Abeta within or around neurons in addition to contributing to NFT formation may also trigger apoptotic pathways. Caspase activation may lead to the cleavage of critical cellular proteins and neuronal cell death associated with DS. (C) 2002 Published by Elsevier Science Ireland Ltd.

引用

页码：99 / 103

页数：5

共 21 条

[1] Morphological and biochemical assessment of DNA damage and apoptosis in Down syndrome and Alzheimer disease, and effect of postmortem tissue archival on TUNEL [J].