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

Prodromal Alzheimer’s Disease: Constitutive Upregulation of Neuroglobin Prevents the Initiation of Alzheimer’s Pathology

3 Dec 2020

Abstract excerpt

In humans, a considerable number of the autopsy samples of cognitively normal individuals aged between 57 and 102 years have revealed the presence of amyloid plaques, one of the typical signs of AD, indicating that many of us use mechanisms that defend ourselves from the toxic consequences of Aß. The human APP NL/F (hAPP NL/F) knockin mouse appears as the ideal mouse model to identify these mechanisms, since they...

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 Hemoglobin structure and function
Share to Protein Structure and Dynamics

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 33343276
DOI: 10.3389/fnins.2020.562581

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Prodromal Alzheimer’s Disease: Constitutive Upregulation of Neuroglobin Prevents the Initiation of Alzheimer’s PathologyPMID 33343276Read ↗

Neuroglobin Protein is Upregulated in Alzheimer's DiseaseSemantic proximity Read ↗

Neuroglobin attenuates beta-amyloid neurotoxicity in vitro and transgenic Alzheimer phenotype in vivo.Semantic proximity Read ↗

APP <sup>NL-F</sup> knock-in Alzheimer’s Disease model mice reveal etiological convergence of aging and amyloidosisSemantic proximity Read ↗

pGluAβ increases accumulation of Aβ in vivo and exacerbates its toxicitySemantic proximity Read ↗

Intraneuronal Aβ accumulation and neurodegeneration: Lessons from transgenic modelsSemantic proximity Read ↗

Pyroglutamate Amyloid-β (Aβ): A Hatchet Man in Alzheimer DiseaseSemantic proximity Read ↗

New <i>App</i> knock-in mice that accumulate wild-type human Aβ as rapidly as <i> App <sup>NL-G-F</sup> </i> mice exhibit intensive cored plaque pathology and neuroinflammationSemantic proximity Read ↗

Soluble Aβ oligomer production and toxicitySemantic proximity Read ↗

Aβ42‐driven cerebral amyloidosis in transgenic mice reveals early and robust pathologySemantic proximity Read ↗

Transgenic animals in Alzheimer's disease research.Semantic proximity Read ↗

Ageing Increases Vulnerability to Aβ42 Toxicity in DrosophilaSemantic proximity Read ↗

Prion-like propagation of β-amyloid aggregates in the absence of APP overexpression.Semantic proximity Read ↗

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