Chrysamine G and its derivative reduce amyloid beta-induced neurotoxicity in mice.

Kazuhiro Ishii, William E Klunk, Shigeki Arawaka, Manik L Debnath, Yoshiko Furiya, Naruhiko Sahara, Shin'ichi Shoji, Akira Tamaoka, Jay W Pettegrew, Hiroshi Mori

文献索引：Neurosci. Lett. 333 , 5-8, (2002)

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摘要

The neurotoxicity of amyloid beta (Abeta) is widely believed to play a seminal role in neurodegeneration in Alzheimer's disease. We examined the effect of Chrysamine G (CG) on such neurotoxicity using the specific measurement of surviving neurons. CG was found to reduce the neurodegeneration induced by both the active short fragment of Abeta(25-35) and full-sized Abeta(1-40). In this study, we synthesized a new chemical compound from a monovalent structure of CG (hCG), with a lower affinity for Abeta, and compared its activity with that of CG. Both CG and hCG were found to be equally efficacious in reducing Abeta-induced neuronal death at a concentration of 0.1-1 microM, indicating that the mechanism of action for CG was not due to its chelating activity, but rather due to its anti-oxidant activity.Copyright 2002 Elsevier Science Ireland Ltd.