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

Yasumasa Ohyagi, Takeshi Yamada, Kenichi Nishioka, Nigel J. Clarke, Andy J. Tomlinson, Stephen Naylor, Yusaku Nakabeppu, Jun Ichi Kira, Steven G. Younkin

研究成果: Contribution to journalArticle査読

65 被引用数 (Scopus)

抄録

Amyloid β protein ending at 42 (Aβ42) plays an important role in the pathology of Alzheimer's disease (AD). Here we show an increase in cellular Aβ42 in damaged neurons, with both ELISA and immunocytochemistry. The cellular Aβ42 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 Aβ was similarly decreased with all these treatments. The cellular Aβ42 increase appeared even with minimal damage (ELISA) and Aβ42-positive cells were TUNEL negative (double staining), indicating that any early apoptosis mechanism may induce the cellular Aβ42 increase. Thus, neuronal apoptosis and cellular Aβ42 increase may be linked in a way that contributes importantly to AD pathology.

本文言語英語
ページ(範囲)167-171
ページ数5
ジャーナルNeuroReport
11
1
DOI
出版ステータス出版済み - 1 17 2000

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

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