Evidence map›Paper›PMID 24498180›Full record

ArticlePloS one2014

A novel acylaminoimidazole derivative, WN1316, alleviates disease progression via suppression of glial inflammation in ALS mouse model.

Kazunori Tanaka, Takuya Kanno, Yoshiko Yanagisawa, Kaori Yasutake, Satoshi Inoue, Noriaki Hirayama, Joh-E Ikeda

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

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 28 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

7 authors at 4 institutions in 2 countries.

Kazunori TanakaNGP Biomedical Research Institute, Neugen Pharma Inc., Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.
Takuya KannoNGP Biomedical Research Institute, Neugen Pharma Inc., Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.
Yoshiko YanagisawaNGP Biomedical Research Institute, Neugen Pharma Inc., Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.
Kaori YasutakeNGP Biomedical Research Institute, Neugen Pharma Inc., Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan.
Satoshi InoueWakunaga Pharmaceutical Co. Ltd., Akitakada, Hiroshima, Japan.
Noriaki HirayamaDepartment of Molecular Life Sciences, Tokai University School of Medicine, Isehara, Kanagawa, Japan.
Joh-E IkedaNGP Biomedical Research Institute, Neugen Pharma Inc., Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan ; Department of Molecular Life Sciences, Tokai University School of Medicine, Isehara, Kanagawa, Japan ; Department of Molecular Neurology, Kitasato University School of Medicine, Sagamihara, Kanagawa, Japan ; Apoptosis Research Centre, Children's Hospital of Eastern Ontario, Department of Pediatrics, Faculty of Medicine, University of Ottawa, Ottawa, Ontario, Canada.
Kitasato University · JPChildren's Hospital of Eastern Ontario · CATokai University · JPWakunaga (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is an adult-onset motor neuron degenerative disease. Given that oxidative stress and resulting chronic neuronal inflammation are thought to be central pathogenic, anti-oxidative agents and modulators of neuronal inflammation could be potential therapies for ALS. We report here that the novel small molecular compound, 2-[mesityl(methyl)amino]-N-[4-(pyridin-2-yl)-1H-imidazol-2-yl] acetamide trihydrochloride (WN1316) selectively suppresses oxidative stress-induced cell death and neuronal inflammation in the late-stage ALS mice. WN1316 has high blood-brain-barrier permeability and water solubility, and boosts both neuronal apoptosis inhibitory protein (NAIP) and NF-E2-related factor 2 (Nrf2) which governed glutathione (GSH)-related anti-oxidation pathway protecting motor neurons against oxidative injuries. Post-onset oral administration of low dose (1-100 µg/kg/day) WN1316 in ALS(SOD1(H46R)) and ALS(SOD1(G93A)) mice resulted in sustained improved motor function and post onset survival rate. Immunohistochemical analysis revealed less DNA oxidative damage and motor neuronal inflammation as well as repression of both microgliosis and astrocytosis, concomitant down regulation of interleukin-1β and inducible nitric oxide synthase, and preservation of the motoneurons in anterior horn of lumbar spinal cord and skeletal muscle (quadriceps femoris). Thus, WN1316 would be a novel therapeutic agent for ALS.

Indexed as

Amyotrophic Lateral SclerosisSpinal CordAnimalsDisease Models, AnimalImidazolesInflammationMiceMuscle, SkeletalNerve Tissue ProteinsImidazolesNerve Tissue Proteins

Identifiers

PMID24498180
PMCPMC3909264
OpenAlexW1986605151

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.