Staurosporine and K-252 compounds protect hippocampal neurons against amyloid β-peptide toxicity and oxidative injury

Yadong Goodman, Mark P. Mattson

Research output: Contribution to journalArticle

Abstract

Recent studies have shown that amyloid β-peptide (Aβ) can be directly neurotoxic by a mechanism related to secondary structure of the peptide, and mediated by free radical production and an increase in the concentration of intracellular free calcium ([Ca2+]i). We now report that staurosporine and K-252 compounds, low molecular weight alkaloids of bacterial origin, can protect cultured rat hippocampal neurons against the toxicity of Aβ in a concentration-dependent manner. The alkaloids also protected neurons against iron-induced (free radical-mediated) injury. Measurements of [Ca2+]i using fura-2 imaging revealed that the elevation of [Ca2+]i that occurred in response to long-term exposure to Aβ was attenuated in neurons treated with staurosporine and K-252 compounds. These findings indicate that staurosporine and K-252 compounds can interupt a neurodegenerative pathway relevant to the pathophysiology of Alzheimer's disease.

Original languageEnglish (US)
Pages (from-to)170-174
Number of pages5
JournalBrain Research
Volume650
Issue number1
DOIs
StatePublished - Jul 4 1994
Externally publishedYes

Keywords

  • Alkaloid
  • Alzheimer's disease
  • Calcium
  • Free radical
  • Fura-2
  • Neurodegeneration
  • Neurotrophic factor
  • Phosphorylation

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

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