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- W3156469684 abstract "Abstract The majority of Alzheimer’s disease (AD) cases are late-onset and occur sporadically, however most mouse models of the disease harbor pathogenic mutations, rendering them better representations of familial autosomal-dominant forms of the disease. Here, we generated knock-in mice that express wildtype human Aβ under control of the mouse App locus. Remarkably, changing 3 amino acids in the mouse Aβ sequence to its wild-type human counterpart leads to age-dependent impairments in cognition and synaptic plasticity, brain volumetric changes, inflammatory alterations, the appearance of Periodic Acid-Schiff (PAS) granules and changes in gene expression. In addition, when exon 14 encoding the Aβ sequence was flanked by loxP sites we show that Cre-mediated excision of exon 14 ablates hAβ expression, rescues cognition and reduces the formation of PAS granules." @default.
- W3156469684 created "2021-04-26" @default.
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- W3156469684 date "2021-04-23" @default.
- W3156469684 modified "2023-10-18" @default.
- W3156469684 title "Generation of a humanized Aβ expressing mouse demonstrating aspects of Alzheimer’s disease-like pathology" @default.
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