Evidence map›Paper›PMID 25025046›Full record

ArticleBioMed research international2014

Chronic neuroinflammation in Alzheimer's disease: new perspectives on animal models and promising candidate drugs.

Christopher Millington, Sandra Sonego, Niloo Karunaweera, Alejandra Rangel, Janice R Aldrich-Wright, Iain L Campbell, Erika Gyengesi, Gerald Münch

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
7.4field-weighted citation impact, top 3% 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

58 citing papers in PubMed, 116 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Christopher MillingtonDepartment of Pharmacology, School of Medicine, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 2751, Australia.
Sandra SonegoDepartment of Pharmacology, School of Medicine, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 2751, Australia.ORCID 0000-0002-4841-0151
Niloo KarunaweeraDepartment of Pharmacology, School of Medicine, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 2751, Australia.ORCID 0000-0002-8798-0990
Alejandra RangelDepartment of Pharmacology, School of Medicine, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 2751, Australia.ORCID 0000-0001-6536-6263
Janice R Aldrich-WrightDepartment of Pharmacology, School of Medicine, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 2751, Australia ; Nanoscale Organisation and Dynamics Group, School of Science and Health, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 2751, Australia.
Iain L CampbellSchool of Molecular Bioscience and the Bosch Institute, University of Sydney, Camperdown, NSW 2006, Australia.
Erika GyengesiDepartment of Pharmacology, School of Medicine, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 2751, Australia.ORCID 0000-0001-7371-7385
Gerald MünchDepartment of Pharmacology, School of Medicine, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 2751, Australia ; Centre for Complementary Medicine Research, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 2751, Australia ; Molecular Medicine Research Group, University of Western Sydney, Locked Bag 1797, Penrith South DC, NSW 2751, Australia.
Western Sydney University · AUThe University of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic neuroinflammation is now considered one of the major factors in the pathogenesis of Alzheimer's disease (AD). However, the most widely used transgenic AD models (overexpressing mutated forms of amyloid precursor protein, presenilin, and/or tau) do not demonstrate the degree of inflammation, neurodegeneration (particularly of the cholinergic system), and cognitive decline that is comparable with the human disease. Hence a more suitable animal model is needed to more closely mimic the resulting cognitive decline and memory loss in humans in order to investigate the effects of neuroinflammation on neurodegeneration. One of these models is the glial fibrillary acidic protein-interleukin 6 (GFAP-IL6) mouse, in which chronic neuroinflammation triggered constitutive expression of the cytokine interleukin-6 (IL-6) in astrocytes. These transgenic mice show substantial and progressive neurodegeneration as well as a decline in motor skills and cognitive function, starting from 6 months of age. This animal model could serve as an excellent tool for drug discovery and validation in vivo. In this review, we have also selected three potential anti-inflammatory drugs, curcumin, apigenin, and tenilsetam, as candidate drugs, which could be tested in this model.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsAstrocytesDisease Models, AnimalGlial Fibrillary Acidic ProteinHumansInflammationInterleukin-6MiceMice, TransgenicNerve Tissue ProteinsAmyloid beta-PeptidesGlial Fibrillary Acidic Proteinglial fibrillary astrocytic protein, mouseInterleukin-6Nerve Tissue Proteins

Identifiers

PMID25025046
PMCPMC4083880
OpenAlexW2011071982

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.