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• W2036638822 abstract "The present commentary based on cell and animal models of intracellular beta-amyloid (iAbeta) expression indicates that low levels of microscopically undetectable iAbeta could have a physiological role in the modulation of the cyclic AMP response element (CRE)-dependent gene expression and, as a consequence, a positive influence on synaptic plasticity (the 'good' Abeta?). On the other hand, high levels of iAbeta resembling the pathological and microscopically visible accumulation of this amyloid peptide, akin to that observed in Down syndrome and Alzheimer's disease, disrupt CRE-regulated gene expression, therefore compromising the protein synthesis-dependent component of long-term potentiation (the 'bad' Abeta?). Moreover, intracellular pathology would be independent and additive to the toxic effects of the extracellular Abeta burden." @default.
• W2036638822 created "2016-06-24" @default.
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• W2036638822 date "2008-01-01" @default.
• W2036638822 modified "2023-10-07" @default.
• W2036638822 title "Impact of Intracellular β-Amyloid in Transgenic Animals and Cell Models" @default.
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• W2036638822 doi "https://doi.org/10.1159/000113686" @default.
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