Evidence map›Paper›PMID 29077059›Full record

ArticleInternational journal of molecular sciences2017

Network-Driven Proteogenomics Unveils an Aging-Related Imbalance in the Olfactory IκBα-NFκB p65 Complex Functionality in Tg2576 Alzheimer's Disease Mouse Model.

Maialen Palomino-Alonso, Mercedes Lachén-Montes, Andrea González-Morales, Karina Ausín, Alberto Pérez-Mediavilla, Joaquín Fernández-Irigoyen, Enrique Santamaría

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.0field-weighted citation impact, top 23% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 16 citations in OpenAlex.

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  11. Molecular and Cellular Mechanisms of Aging and Age-related Disorders.International journal of molecular sciences · 2018
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Maialen Palomino-AlonsoClinical Neuroproteomics Group, Navarrabiomed, Departamento de Salud, Universidad Pública de Navarra, 31008 Pamplona, Spain. mpalomino@alumni.unav.es.
Mercedes Lachén-MontesClinical Neuroproteomics Group, Navarrabiomed, Departamento de Salud, Universidad Pública de Navarra, 31008 Pamplona, Spain. mercedes.lachen.montes@navarra.es.
Andrea González-MoralesClinical Neuroproteomics Group, Navarrabiomed, Departamento de Salud, Universidad Pública de Navarra, 31008 Pamplona, Spain. andrea.gonzalez.morales@navarra.es.
Karina AusínProteored-ISCIII, Proteomics Unit, Navarrabiomed, Departamento de Salud, Universidad Pública de Navarra, 31008 Pamplona, Spain. karina.ausin.perez@navarra.es.
Alberto Pérez-MediavillaInstituto de Investigación Sanitaria de Navarra (IdiSNA), Navarra Institute for Health Research, 31008 Pamplona, Spain. lamediav@unav.es.
Joaquín Fernández-IrigoyenClinical Neuroproteomics Group, Navarrabiomed, Departamento de Salud, Universidad Pública de Navarra, 31008 Pamplona, Spain. jokfer@gmail.com.
Enrique SantamaríaClinical Neuroproteomics Group, Navarrabiomed, Departamento de Salud, Universidad Pública de Navarra, 31008 Pamplona, Spain. esantamma@navarra.es.
Universidad Publica de Navarra · ESNavarre Institute of Health Research · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Olfaction is often deregulated in Alzheimer's disease (AD) patients, and is also impaired in transgenic Tg2576 AD mice, which overexpress the Swedish mutated form of human amyloid precursor protein (APP). However, little is known about the molecular mechanisms that accompany the neurodegeneration of olfactory structures in aged Tg2576 mice. For that, we have applied proteome- and transcriptome-wide approaches to probe molecular disturbances in the olfactory bulb (OB) dissected from aged Tg2576 mice (18 months of age) as compared to those of age matched wild-type (WT) littermates. Some over-represented biological functions were directly relevant to neuronal homeostasis and processes of learning, cognition, and behavior. In addition to the modulation of CAMP responsive element binding protein 1 (CREB1) and APP interactomes, an imbalance in the functionality of the IκBα-NFκB p65 complex was observed during the aging process in the OB of Tg2576 mice. At two months of age, the phosphorylated isoforms of olfactory IκBα and NFκB p65 were inversely regulated in transgenic mice. However, both phosphorylated proteins were increased at 6 months of age, while a specific drop in IκBα levels was detected in 18-month-old Tg2576 mice, suggesting a transient activation of NFκB in the OB of Tg2576 mice. Taken together, our data provide a metabolic map of olfactory alterations in aged Tg2576 mice, reflecting the progressive effect of APP overproduction and β-amyloid (Aβ) accumulation on the OB homeostasis in aged stages.

Indexed as

ProteogenomicsAge FactorsAlzheimer DiseaseAnimalsCluster AnalysisDisease Models, AnimalFemaleGene Expression ProfilingGene Regulatory NetworksI-kappa B ProteinsMiceMice, TransgenicNeuronsOlfactory BulbOrgan SpecificityProtein Interaction MapsI-kappa B ProteinsProteomeTranscription Factor RelAmass-spectrometryolfactory bulbproteogenomicsTg2576 mice

Identifiers

PMID29077059
PMCPMC5713230
OpenAlexW2766725060

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.