Apoptosis induced by β-amyloid25-35 in acetylcholinesterase-overexpressing neuroblastoma cells

Hai Yan Zhang, Stephen Brimijoin, Xi Can Tang

Research output: Contribution to journalArticlepeer-review

14 Scopus citations


AIM: To examine the relationship between apoptosis induced by β-amyloid fragment 25-35 (Aβ25-35) and the activity of acetylcholinesterase (AChE) in AChE over-expresser-SC42 cells. METHODS: Cell survival was measured by microscopy and MTT reduction; DNA laddering was observed by electrophoresis; AChE activity was determined by spectrophotometry. RESULTS: Aβ25-35 1 μmol/L exposure for 24-48 h caused a significant decrease in cell viability, along with changes in morphology and DNA fragmentation. AChE activity was affected in an inverse manner, increasing gradually to a level that was 1.7-fold higher than control at the 48-h time point. No change in the cytotoxicity of Aβ25-35 was observed when the increased AChE activities were effectively inhibited by huperzine A throughout the 48-h exposure period. CONCLUSION: Although Aβ 25-35 can induce apoptosis in SC42 cells and simultaneously increase AChE activity, the capacity of AChE to hydrolyze acetylcholine is not involved in this apoptosis model.

Original languageEnglish (US)
Pages (from-to)853-958+948
JournalActa Pharmacologica Sinica
Issue number9
StatePublished - Sep 1 2003


  • Acetylcholinesterase
  • Amyloid beta protein
  • Apoptosis
  • SC35 cells
  • SC42 cells

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)


Dive into the research topics of 'Apoptosis induced by β-amyloid25-35 in acetylcholinesterase-overexpressing neuroblastoma cells'. Together they form a unique fingerprint.

Cite this