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- W2049144486 abstract "The beta-amyloid precursor protein (beta-APP), from which the beta-A4 peptide is derived, is considered to be central to the pathogenesis of Alzheimer disease (AD). Transgenic mice expressing the 751-amino acid isoform of human beta-APP (beta-APP751) have been shown to develop early AD-like histopathology with diffuse deposits of beta-A4 and aberrant tau protein expression in the brain, particularly in the hippocampus, cortex, and amygdala. We now report that beta-APP751 transgenic mice exhibit age-dependent deficits in spatial learning in a water-maze task and in spontaneous alternation in a Y maze. These deficits were mild or absent in 6-month-old transgenic mice but were severe in 12-month-old transgenic mice compared to age-matched wild-type control mice. No other behavioral abnormalities were observed. These mice therefore model the progressive learning and memory impairment that is a cardinal feature of AD. These results provide evidence for a relationship between abnormal expression of beta-APP and cognitive impairments." @default.
- W2049144486 created "2016-06-24" @default.
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- W2049144486 date "1995-06-06" @default.
- W2049144486 modified "2023-09-25" @default.
- W2049144486 title "Age-related learning deficits in transgenic mice expressing the 751-amino acid isoform of human beta-amyloid precursor protein." @default.
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- W2049144486 doi "https://doi.org/10.1073/pnas.92.12.5341" @default.
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