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

Beneficial effects of the β-secretase inhibitor GRL-8234 in 5XFAD Alzheimer's transgenic mice lessen during disease progression.

Current Alzheimer research - 1 Jan 2015

Devi Latha, Tang Jordan, Ohno Masuo

Abstract excerpt

The β-secretase enzyme BACE1, which initiates the cleavage of amyloid precursor protein (APP) into the amyloid-β (Aβ) peptide, is a prime therapeutic target for Alzheimer's disease (AD). However, recent investigations using genetic animal models raise concern that therapeutic BACE1 inhibition may encounter the dramatic reduction of efficacy in ameliorating AD-like pathology and memory deficits during disease...

Read the complete abstract on PubMed

Topics

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

Share to Amyloid beta-Peptides
Share to Amyloid beta-Protein Precursor

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Amyloid Precursor Protein Secretases

Share to Amyloidosis

Share to Cerebral Cortex

Share to Maze Learning

Share to Presenilin-1

Share to Sulfonamides

Source

Open in PubMed Open full text

Identifiers

PMID: 25523425
DOI: 10.2174/1567205012666141218125042
PMCID: PMC4414026

Genes

BACE1
APP

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Beneficial effects of the β-secretase inhibitor GRL-8234 in 5XFAD Alzheimer's transgenic mice lessen during disease progression.PMID 25523425Read ↗

Phospho-eIF2α Level Is Important for Determining Abilities of BACE1 Reduction to Rescue Cholinergic Neurodegeneration and Memory Defects in 5XFAD MiceSemantic proximity Read ↗

Behavioral and neural network abnormalities in human APP transgenic mice resemble those of App knock-in mice and are modulated by familial Alzheimer's disease mutations but not by inhibition of BACE1.Semantic proximity Read ↗

Partial reduction of BACE1 improves synaptic plasticity, recent and remote memories in Alzheimer's disease transgenic mice.Semantic proximity Read ↗

Behavioral phenotypes of amyloid-based genetically modified mouse models of Alzheimer's disease.Semantic proximity Read ↗

Knock-in of human BACE1 cleaves murine APP and reiterates Alzheimer-like phenotypes.Semantic proximity Read ↗

Effects of BACE1 haploinsufficiency on APP processing and Aβ concentrations in male and female 5XFAD Alzheimer mice at different disease stages.Semantic proximity Read ↗

Rodent models for Alzheimer’s disease drug discoverySemantic proximity Read ↗

Centrally Delivered BACE1 Inhibitor Activates Microglia, and Reverses Amyloid Pathology and Cognitive Deficit in Aged Tg2576 Mice.Semantic proximity Read ↗

Leveraging preclinical models for the development of Alzheimer disease therapeutics.Semantic proximity Read ↗

A novel BACE inhibitor NB-360 shows a superior pharmacological profile and robust reduction of amyloid-β and neuroinflammation in APP transgenic mice.Semantic proximity Read ↗

Presenilin-1 but not amyloid precursor protein mutations present in mouse models of Alzheimer's disease attenuate the response of cultured cells to γ-secretase modulators regardless of their potency and structure.Semantic proximity Read ↗

Identification and drug-induced reversion of molecular signatures of Alzheimer’s disease onset and progression in AppNL-G-F, AppNL-F, and 3xTg-AD mouse modelsSemantic proximity Read ↗

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