期刊
NEUROREPORT
卷 11, 期 1, 页码 167-171出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00001756-200001170-00033
关键词
amyloid beta protein; apoptosis; ELISA; immunocytochemistry; increase; necrosis; neuron
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.
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