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

Research output: Contribution to journalArticlepeer-review

65 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)167-171
Number of pages5
JournalNeuroReport
Volume11
Issue number1
DOIs
StatePublished - Jan 17 2000

Keywords

  • Amyloid β protein
  • Apoptosis
  • ELISA
  • Immunocytochemistry
  • Increase
  • Necrosis
  • Neuron

ASJC Scopus subject areas

  • Neuroscience(all)

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