Increased Level of beta-Amyloid in the Brain of Bulbectomized Mice

I. Yu. Aleksandrova¹, V. V. Kuvichkin¹, I. A. Kashparov², N. I. Medvinskaya¹, I. V. Nesterova¹, S. M. Lunin¹, A. N. Samokhin¹, and N. V. Bobkova^1*

¹Institute of Cell Biophysics, Russian Academy of Sciences, Pushchino 142290, Moscow Region, Russia; fax: (0967) 33-0509; E-mail: nbobkova@mail.ru

²Protein Institute, Russian Academy of Sciences, Pushchino 142290, Moscow Region, Russia; fax: (7-095) 924-049

^* To whom correspondence should be addressed.

Received January 23, 2003; Revision received June 17, 2003

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Six weeks after bilateral olfactory bulbectomy, a peptide with molecular weight of 4 kD was revealed in extracts of the neocortex and hippocampus from mice. Using monoclonal antibodies 4G8, this peptide was identified as beta-amyloid. Its level was significantly higher in the bulbectomized animals than in sham-operated mice. The bulbectomized mice displayed sharp impairment in spatial memory when tested in the Morris water maze. The results suggest that bulbectomy initiates in the brain a pathological process similar to human Alzheimer's disease in location, biochemistry, and behavioral manifestations.

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KEY WORDS: sporadic Alzheimer's disease, animal models of human diseases, bulbectomy, beta-amyloid, spatial memory

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