β-Amyloid precursor polypeptide in SAMP8 mice affects learning and memory
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Morley, JE
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St Louis Dept Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, St Louis, MO 63104 USASt Louis Dept Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, St Louis, MO 63104 USA
Morley, JE
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Kumar, VB
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机构:St Louis Dept Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, St Louis, MO 63104 USA
Kumar, VB
Bernardo, AE
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机构:St Louis Dept Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, St Louis, MO 63104 USA
Bernardo, AE
Farr, SA
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机构:St Louis Dept Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, St Louis, MO 63104 USA
Farr, SA
Uezu, K
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Uezu, K
Tumosa, N
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Tumosa, N
Flood, JF
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机构:St Louis Dept Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, St Louis, MO 63104 USA
Flood, JF
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[1] St Louis Dept Vet Affairs Med Ctr, Ctr Geriatr Res Educ & Clin, St Louis, MO 63104 USA
[2] St Louis Univ, Hlth Sci Ctr, Div Geriatr Med, St Louis, MO 63104 USA
Senescence accelerated (SAMP8 [P8]) mice develop age related deficits in memory and learning. We show that increased expression of amyloid precursor protein (APP) and its mRNA in the hippocampus are also age-related. Immunocytochemical data suggest that a critical amount of APP expression may be needed to generate amyloid (A beta) protein plaques in the hippocampus. Deficits in acquisition and retention test performance were alleviated by administration of antibody to A beta protein into the cerebral ventricles. This revel-sai of cognitive deficits provides a link between increased expression of both APP and A beta protein and learning and memory loss in these mice. (C) 2000 Published by Elsevier science Inc.