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

Delta-secretase triggers Alzheimer’s disease pathologies in wild-type hAPP/hMAPT double transgenic mice

12 Dec 2020

Abstract excerpt

Alzheimer's disease (AD) is the most common neurodegenerative disease with multifactorial pathologies including Aβ containing senile plaques and neurofibrillary tangles (NFT) consisted of aggregated Tau. Most of the AD patients are sporadic and the familial mutation hereditary patients are composed only 1% of all cases. However, the current AD mouse models employ mutated APP, PS1, or even Tau mutant, in order to...

Read the complete abstract on PubMed

Topics

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

Share to Alzheimer's disease research and treatments
Share to Peptidase Inhibition and Analysis
Share to Protein Hydrolysis and Bioactive Peptides

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 33311478
DOI: 10.1038/s41419-020-03270-7

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Delta-secretase triggers Alzheimer’s disease pathologies in wild-type hAPP/hMAPT double transgenic micePMID 33311478Read ↗

C/EBPβ regulates delta-secretase expression and mediates pathogenesis in mouse models of Alzheimer’s diseaseSemantic proximity Read ↗

Pathogenic Aβ generation in familial Alzheimer's disease: novel mechanistic insights and therapeutic implications.Semantic proximity Read ↗

Mouse models of Alzheimer's disease: The long and filamentous roadSemantic proximity Read ↗

Presenilin, γ-Secretase, and the Search for Pathogenic Triggers of Alzheimer's Disease.Semantic proximity Read ↗

The Uppsala APP Mutation Promotes Wild-Type Amyloid-β Aggregation and Deposition In Vivo.Semantic proximity Read ↗

Deletion of the γ-secretase subunits Aph1B/C impairs memory and worsens the deficits of knock-in mice modeling the Alzheimer-like familial Danish dementia.Semantic proximity Read ↗

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

Expression of endogenous mouse APP modulates β-amyloid deposition in hAPP-transgenic mice.Semantic proximity Read ↗

AHA1 regulates Aβ production via modulation of APP expression and γ-secretase assemblySemantic proximity Read ↗

Emerging roles of N- and C-terminally truncated Aβ species in Alzheimer’s diseaseSemantic proximity Read ↗

A{beta} accelerates the spatiotemporal progression of tau pathology and augments tau amyloidosis in an Alzheimer mouse model.Semantic proximity Read ↗

Deposition of C-terminally truncated Aβ species Aβ37 and Aβ39 in Alzheimer's disease and transgenic mouse models.Semantic proximity Read ↗

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