Evidence map›Paper›PMID 36153399›Full record

ArticleScientific reports2022

Melatonin ameliorates disease severity in a mouse model of multiple sclerosis by modulating the kynurenine pathway.

Yahya Jand, Mohammad Hossein Ghahremani, Amir Ghanbari, Shahram Ejtemaei-Mehr, Gilles J Guillemin, Mahmoud Ghazi-Khansari

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
3.6field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

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  5. Deciphering the role of nicotinamide metabolism and melanin-related genes in acute myocardial infarction: a machine learning approach integrating bioinformatics analysis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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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

6 authors at 3 institutions in 2 countries.

Yahya JandDepartment of Pharmacology, School of Medicine, Tehran University of Medical Sciences, P.O. Box 13145-784, Tehran, Iran.
Mohammad Hossein GhahremaniDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, University of Medical Sciences, Tehran, Iran.
Amir GhanbariCellular and Molecular Research Center, Yasuj University of Medical Sciences, Yasuj, Iran.
Shahram Ejtemaei-MehrDepartment of Pharmacology, School of Medicine, Tehran University of Medical Sciences, P.O. Box 13145-784, Tehran, Iran.
Gilles J GuilleminNeuroinflammation Group, Faculty of Medicine and Health Sciences, Macquarie University, Sydney, NSW, Australia.
Mahmoud Ghazi-KhansariDepartment of Pharmacology, School of Medicine, Tehran University of Medical Sciences, P.O. Box 13145-784, Tehran, Iran. ghazikha@tums.ac.ir.
Tehran University of Medical Sciences · IRMacquarie University · AUYasuj University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Melatonin (MT), a neurohormone with immunomodulatory properties, is one of the metabolites produced in the brain from tryptophan (TRP) that has already strong links with the neuropathogenesis of Multiple sclerosis (MS). However, the exact molecular mechanisms behind that are not fully understood. There is some evidence showing that MS and MT are interconnected via different pathways: Relapses of MS has a direct correlation with a low level of MT secretion and a growing body of evidence suggest that MT be therapeutic in Experimental Autoimmune Encephalomyelitis (EAE, a recognise animal model of MS) severity. Previous studies have demonstrated that the kynurenine pathway (KP), the main pathway of TRP catabolism, plays a key role in the pathogenesis of MS in humans and in EAE. The present study aimed to investigate whether MT can improve clinical signs in the EAE model by modulating the KP. C57BL/6 mice were induced with EAE and received different doses of MT. Then the onset and severity of EAE clinical symptoms were recorded. Two biological factors, aryl hydrocarbon receptor (AhR) and NAD

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMelatoninMultiple SclerosisAnimalsBiological FactorsDisease Models, AnimalHumansIndoleamine-Pyrrole 2,3,-DioxygenaseKynurenineMiceMice, Inbred C57BLNADNicotinamide N-MethyltransferaseReceptors, Aryl HydrocarbonRNA, MessengerSeverity of Illness IndexBiological FactorsIndoleamine-Pyrrole 2,3,-DioxygenaseKynurenineMelatoninNADNicotinamide N-MethyltransferaseReceptors, Aryl HydrocarbonRNA, MessengerTryptophan

Identifiers

PMID36153399
PMCPMC9509376
OpenAlexW4296935340

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.