Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Genetic cathepsin B deficiency reduces beta-amyloid in transgenic mice expressing human wild-type amyloid precursor protein.

Biochemical and biophysical research communications - 21 Aug 2009

Hook Vivian Y H, Kindy Mark, Reinheckel Thomas, Peters Christoph, Hook Gregory

Abstract excerpt

Neurotoxic beta-amyloid (Abeta) peptides participate in Alzheimer's disease (AD); therefore, reduction of Abeta generated from APP may provide a therapeutic approach for AD. Gene knockout studies in transgenic mice producing human Abeta may identify targets for reducing Abeta. This study shows that knockout of the cathepsin B gene in mice expressing human wild-type APP (hAPPwt) results in substantial decreases in...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Alzheimer Disease
Share to Amyloid beta-Peptides

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Amyloid beta-Protein Precursor

Share to Cathepsin B

Share to Gene Knockout Techniques

Share to Mice, Transgenic

Share to Peptide Fragments

Source

Open in PubMed Open full text

Identifiers

PMID: 19501042
DOI: 10.1016/j.bbrc.2009.05.131
PMCID: PMC2753505

Genes

APP

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026. Manifest publication-graph-cohort-2026-09-05.1.

Source receipt: pubmed, retrieved 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Genetic cathepsin B deficiency reduces beta-amyloid in transgenic mice expressing human wild-type amyloid precursor protein.PMID 19501042Read ↗

Cathepsin B degrades amyloid-β in mice expressing wild-type human amyloid precursor protein.Semantic proximity Read ↗

Antiamyloidogenic and neuroprotective functions of cathepsin B: implications for Alzheimer's disease.Semantic proximity Read ↗

Deletion of the cathepsin B gene improves memory deficits in a transgenic ALZHeimer's disease mouse model expressing AβPP containing the wild-type β-secretase site sequence.Semantic proximity Read ↗

Enhanced amyloidogenic processing of the beta-amyloid precursor protein in gene-targeted mice bearing the Swedish familial Alzheimer's disease mutations and a "humanized" Abeta sequence.Semantic proximity Read ↗

Amyloid precursor protein transgenic mouse models and Alzheimer's disease: Understanding the paradigms, limitations, and contributionsSemantic proximity Read ↗

An isogenic panel of single <i>App</i> knock-in mouse models of Alzheimer’s disease confers differential profiles of β-secretase inhibition and endosomal abnormalitiesSemantic proximity Read ↗

APP transgenic modeling of Alzheimer's disease: mechanisms of neurodegeneration and aberrant neurogenesis.Semantic proximity Read ↗

Single App knock-in mouse models of Alzheimer's disease.Semantic proximity Read ↗

An isogenic panel of App knock-in mouse models: Profiling β-secretase inhibition and endosomal abnormalitiesSemantic proximity Read ↗

Wild type and mutant amyloid precursor proteins influence downstream effects of proteasome and autophagy inhibition.Semantic proximity Read ↗

Cat and mouse.Semantic proximity Read ↗

The effects of parkin suppression on the behaviour, amyloid processing, and cell survival in APP mutant transgenic mice.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.