Toxic effect of a beta-amyloid peptide (beta 22-35) on the hippocampal neuron and its prevention.
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.
Takadera
T
T
Faculty of Pharmaceutical Sciences, Hokuriku University, Kanazawa, Japan.
Sakura
N
N
Mohri
T
T
Hashimoto
T
T
D016229:Amyloid beta-Peptides / Q000633:toxicity*; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D002478:Cells, Cultured; D006624:Hippocampus / Q000187:drug effects*; D007328:Insulin / Q000494:pharmacology; D009414:Nerve Growth Factors / Q000494:pharmacology; D009474:Neurons / Q000187:drug effects; D051381:Rats; D013373:Substance P / Q000494:pharmacology
D016229:Amyloid beta-Peptides; D007328:Insulin; D009414:Nerve Growth Factors; D013373:Substance P; D003994:Bucladesine