Amyloid-β1-42M induces reactive oxygen species-mediated autophagic cell death in U87 and SH-SY5Y cells

Hongmei Wang, Jianfang Ma, Yuyan Tan, Zhiquan Wang, Chengyu Sheng, Shengdi Chen, Jianqing Ding

Research output: Contribution to journalArticlepeer-review

64 Scopus citations


Alzheimer's disease (AD) is a neurodegenerative disorder initiated by the aggregation of amyloid-β peptide (Aβ). Macroautophagy, which is essential for cell survival as well as the promotion of cell death, has been observed extensively in AD brains or transgenic mice overexpressing Aβ protein precursor. However, the role of macroautophagy in the pathogenesis of AD is unclear. In this study, we showed that Aβ1-42 triggered autophagic cell death in both human glioma cell line (U87 cell) and human neuroblastoma cell line (SH-SY5Y cell). Aβ1-42-induced cytotoxicity and autophagic cell death were blocked by the autophagy inhibitor 3-methyladenine (3-MA) or by small interfering RNA against the autophagy gene Beclin-1. Reactive oxygen species (ROS) accumulation was also detected in both Aβ1-42 treated cell lines and this accumulation was not affected by 3-MA. Moreover, pretreatment with the ROS scavenger N-acetylcysteine inhibited ROS accumulation and autophagic cell death induced by Aβ1-42, suggesting that Aβ1-42-induced ROS accumulation might trigger the onset of autophagy and subsequent autophagic cell death. These findings provide further insights into the mechanisms underlying Aβ-induced cytotoxicity.

Original languageEnglish (US)
Pages (from-to)597-610
Number of pages14
JournalJournal of Alzheimer's Disease
Issue number2
StatePublished - 2010


  • Apoptosis
  • Beclin-1
  • N-acetylcysteine
  • autophagic cell death
  • reactive oxygen species

ASJC Scopus subject areas

  • General Neuroscience
  • Clinical Psychology
  • Geriatrics and Gerontology
  • Psychiatry and Mental health


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