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Article

Knock-in of human BACE1 cleaves murine APP and reiterates Alzheimer-like phenotypes.

The Journal of neuroscience : the official journal of the Society for Neuroscience - 6 Aug 2014

Plucińska Kaja, Crouch Barry, Koss David, Robinson Lianne, Siebrecht Michael, Riedel Gernot, Platt Bettina

Abstract excerpt

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...

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Source

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Identifiers

PMID: 25100603
DOI: 10.1523/JNEUROSCI.0433-14.2014
PMCID: PMC4122804

Genes

APP
BACE1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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