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• W2020131301 abstract "Key neuropathological hallmarks of Alzheimer's disease (AD) are elevated levels of amyloid β-peptide (Aβ) species generated via amyloid precursor protein (APP) endoproteolysis and cleavage by the rate-limiting β-site enzyme 1 (BACE1). Because rodents do not develop amyloid pathologies, we here investigated whether AD-like endophenotypes can be created in mice by expression of human bace1. To avoid pitfalls of existing models, we introduced hbace1 via knock-in under the control of the CaMKII α promoter into the safe HPRT locus. We report amyloidogenic processing of murine APP in the hBACE1 mice (termed PLB4), resulting in the formation of toxic APP metabolites that accumulate intra- and extraneuronally in hippocampus and cortex. Pronounced accumulation of Aβ*56 and Aβ hexamers in the absence of plaque deposition was detected in brain tissue from symptomatic PLB4 mice. Heightened levels of inflammation (gliosis) also appeared in several AD-related brain regions (dentate gyrus, hippocampal area CA1, piriform and parietal cortices) at 6 and 12 months of age. Behaviorally, deficits in habituation to a novel environment and semantic-like memory (social transmission of food preference) were detected from 3 to 4 months of age. Impairments in spatial learning strategies in long-term reference (water maze) and working memory (Y-maze) tasks presented at 6 months, and were distinct from reductions in locomotor activity and anxiety. Overall, our data indicate for the first time that targeted, subtle forebrain-specific expression through single gene knock-in of hBACE1 is sufficient to generate AD-relevant cognitive impairments amid corresponding histopathologies, confirming human BACE as the key parameter in amyloid pathogenesis." @default.
• W2020131301 created "2016-06-24" @default.
• W2020131301 creator A5002411835 @default.
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• W2020131301 date "2014-08-06" @default.
• W2020131301 modified "2023-10-18" @default.
• W2020131301 title "Knock-In of Human BACE1 Cleaves Murine APP and Reiterates Alzheimer-like Phenotypes" @default.
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• W2020131301 doi "https://doi.org/10.1523/jneurosci.0433-14.2014" @default.
• W2020131301 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4122804" @default.
• W2020131301 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25100603" @default.
• W2020131301 hasPublicationYear "2014" @default.
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