Toxic effect of a beta-amyloid peptide (beta 22-35) on the hippocampal neuron and its prevention

Neurosci Lett. 1993 Oct 14;161(1):41-4. doi: 10.1016/0304-3940(93)90135-8.


A synthetic truncated beta-amyloid peptide, beta 22-35, was shown to have a cytotoxic effect on cultured neurons from the rat hippocampus in serum-free medium. The peptide formed aggregates and typical amyloid fibrils resembling those of the beta-amyloid protein (AP) in neutral buffer solution and showed characteristic staining with Congo red and thioflavin-S. The neurotoxicity of beta 22-35 was suppressed by addition of calf serum, dibutyryl cAMP or insulin to culture medium, but not by addition of NGF or substance P. beta 22-35 had no effect on the glial cells. These results suggest that the AP can induce neurotoxicity in the hippocampal cells in vitro and the toxicity may involve a disorder in the intracellular signal transduction.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid beta-Peptides / toxicity*
  • Animals
  • Bucladesine / pharmacology
  • Cells, Cultured
  • Hippocampus / drug effects*
  • Insulin / pharmacology
  • Nerve Growth Factors / pharmacology
  • Neurons / drug effects
  • Rats
  • Substance P / pharmacology


  • Amyloid beta-Peptides
  • Insulin
  • Nerve Growth Factors
  • Substance P
  • Bucladesine