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Gerontology. 1996;42 Suppl 1:48-56.

Systemic overexpression of a C-terminal fragment of human amyloid beta-protein precursor causes accumulation of Alzheimer beta-amyloid fibrils in pancreas of transgenic mice.

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  • 1Department of Neurology, Gunma University School of Medicine, Maebashi, Japan.


The deposition of amyloid beta-protein (A beta), derived from amyloid beta-protein precursor (beta APP), is a specific and early event in development of Alzheimer's disease. Transgenic mice carrying the carboxyl-terminus of beta APP gene linked to the cytomegalovirus enhancer/chicken beta-actin promoter sequence were studied. Deposition of amyloid fibrils, composing A beta, was observed in the transgenic pancreas, accompanied with cell degeneration. This result will provide a model to investigate the beta APP processing mechanism in vivo and a clue to generate possible A beta amyloidosis in animal brains.

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