Selective increase in cellular Aβ42 is related to apoptosis but not necrosis

被引：67

作者：

Ohyagi, Y

Yamada, T

Nishioka, K

Clarke, NJ

Tomlinson, AJ

Naylor, S

Nakabeppu, Y

Kira, J

Younkin, SG

机构：

[1] Mayo Clin Jacksonville, Dept Pharmacol, Jacksonville, FL 32224 USA

[2] Kyushu Univ, Grad Sch Med Sci, Neurol Inst, Dept Neurol,Higashi Ku, Fukuoka 8128582, Japan

[3] Kyushu Univ, Med Inst Bioregulat, Dept Biochem, Higashi Ku, Fukuoka 8128582, Japan

[4] Mayo Clin Rochester, Dept Biochem & Mol Biol, Biomed Mass Spectrometry Facil, Rochester, MN 55905 USA

来源：

NEUROREPORT | 2000年 / 11卷 / 01期

关键词：

amyloid beta protein; apoptosis; ELISA; immunocytochemistry; increase; necrosis; neuron;

D O I：

10.1097/00001756-200001170-00033

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Amyloid beta protein ending at 42 (A beta 42) plays an important role in the pathology of Alzheimer's disease (AD). Here we show an increase in cellular A beta 42 in damaged neurons, with both ELISA and immunocytochemistry. The cellular A beta 42 increase was caused by 3-day treatments with H2O2. etoposide or melphalan, all of which induce genotoxic apoptosis, but not by treatment with sodium azide, which causes necrosis. Secreted A beta was similarly decreased with all these treatments. The cellular A beta 42 increase appeared even with minimal damage (ELISA) and A beta 42-positive cells were TUNEL negative (double staining), indicating that any early apoptosis mechanism may induce the cellular A beta 42 increase. Thus, neuronal apoptosis and cellular A beta 42 increase may be linked in a way that contributes importantly to AD pathology. NeuroReport 11:167-171 (C) 2000 Lippincott Williams & Wilkins.

引用

收藏

页码：167 / 171

页数：5

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