Evidence map›Paper›PMID 30666558›Full record

ArticleNeurotoxicity research2019

Kynurenine 3-Monooxygenase Activity in Human Primary Neurons and Effect on Cellular Bioenergetics Identifies New Neurotoxic Mechanisms.

Gloria Castellano-Gonzalez, Kelly R Jacobs, Emily Don, Nicholas J Cole, Seray Adams, Chai K Lim, David B Lovejoy, Gilles J Guillemin

Abstract read
PubMed Publisher
In one paragraph

Article in Neurotoxicity research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

36 citing papers in PubMed, 49 citations in OpenAlex.

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  18. PTSD, Immune System, and Inflammation.Advances in experimental medicine and biology · 2023
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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 1 institution in 1 country.

Gloria Castellano-GonzalezNeuroinflammation Group, Centre for Motor Neuron Disease Research, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences (FMHS), Macquarie University, 2, Technology Place, North Ryde, NSW, 2109, Australia.
Kelly R JacobsNeuroinflammation Group, Centre for Motor Neuron Disease Research, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences (FMHS), Macquarie University, 2, Technology Place, North Ryde, NSW, 2109, Australia.
Emily DonCentre for Motor Neuron Disease Research, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences (FMHS), Macquarie University, North Ryde, NSW, 2109, Australia.
Nicholas J ColeCentre for Motor Neuron Disease Research, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences (FMHS), Macquarie University, North Ryde, NSW, 2109, Australia.
Seray AdamsNeuroinflammation Group, Centre for Motor Neuron Disease Research, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences (FMHS), Macquarie University, 2, Technology Place, North Ryde, NSW, 2109, Australia.
Chai K LimNeuroinflammation Group, Centre for Motor Neuron Disease Research, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences (FMHS), Macquarie University, 2, Technology Place, North Ryde, NSW, 2109, Australia.
David B LovejoyNeuroinflammation Group, Centre for Motor Neuron Disease Research, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences (FMHS), Macquarie University, 2, Technology Place, North Ryde, NSW, 2109, Australia. david.lovejoy@mq.edu.au.
Gilles J GuilleminNeuroinflammation Group, Centre for Motor Neuron Disease Research, Department of Biomedical Sciences, Faculty of Medicine and Health Sciences (FMHS), Macquarie University, 2, Technology Place, North Ryde, NSW, 2109, Australia. gilles.guillemin@mq.edu.au.
Macquarie University · AU

Funding

Australian Research Council N/AMacquarie University N/A
6 · The paper itself

Abstract

Upregulation of the kynurenine pathway (KP) of tryptophan metabolism is commonly observed in neurodegenerative disease. When activated, L-kynurenine (KYN) increases in the periphery and central nervous system where it is further metabolised to other neuroactive metabolites including 3-hydroxykynurenine (3-HK), kynurenic acid (KYNA) and quinolinic acid (QUIN). Particularly biologically relevant metabolites are 3-HK and QUIN, formed downstream of the enzyme kynurenine 3-monooxygenase (KMO) which plays a pivotal role in maintaining KP homeostasis. Indeed, excessive production of 3-HK and QUIN has been described in neurodegenerative disease including Alzheimer's disease and Huntington's disease. In this study, we characterise KMO activity in human primary neurons and identified new mechanisms by which KMO activation mediates neurotoxicity. We show that while transient activation of the KP promotes synthesis of the essential co-enzyme nicotinamide adenine dinucleotide (NAD

Indexed as

Adenosine TriphosphateBrainCell SurvivalHEK293 CellsHumansKynurenic AcidKynurenineKynurenine 3-MonooxygenaseMembrane Potential, MitochondrialMitochondriaMitochondrial DiseasesNADNeuronsOxidative StressPrimary Cell CultureQuinolinic Acid3-hydroxykynurenineAdenosine TriphosphateKynurenic AcidKynurenineKynurenine 3-MonooxygenaseNADQuinolinic AcidReactive Oxygen SpeciesKynurenine 3-monooxygenaseKynurenine pathwayMitochondrial dysfunctionOxidative stress

Identifiers

PMID30666558
OpenAlexW2912873508

What OpenQuestion holds

Textmetadata
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.