Evidence map›Paper›PMID 25562842›Full record

ArticleTranslational psychiatry2015

N-Acetylcysteine improves mitochondrial function and ameliorates behavioral deficits in the R6/1 mouse model of Huntington's disease.

D J Wright, T Renoir, Z M Smith, A E Frazier, P S Francis, D R Thorburn, S L McGee, A J Hannan, L J Gray

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

Article in Translational psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

69 citing papers in PubMed, 134 citations in OpenAlex.

  1. Review
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  6. Hydrogen Sulfide Signaling in Neurodegenerative Movement Disorders.Handbook of experimental pharmacology · 2026
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9 more citing papers are in PubMed but not listed here.

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

9 authors at 2 institutions in 1 country.

D J Wright1] Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, Australia [2] School of Medicine, Faculty of Health, Deakin University, Geelong, VIC, Australia.
T RenoirFlorey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, Australia.
Z M SmithCentre for Chemistry and Biotechnology, Faculty of Science, Engineering and Built Environment, Deakin University, Geelong, VIC, Australia.
A E Frazier1] Murdoch Childrens Research Institute, Royal Children's Hospital, Melbourne, VIC, Australia [2] Department of Paediatrics, University of Melbourne, Parkville, VIC, Australia.
P S FrancisCentre for Chemistry and Biotechnology, Faculty of Science, Engineering and Built Environment, Deakin University, Geelong, VIC, Australia.
D R Thorburn1] Murdoch Childrens Research Institute, Royal Children's Hospital, Melbourne, VIC, Australia [2] Department of Paediatrics, University of Melbourne, Parkville, VIC, Australia [3] Victorian Clinical Genetics Services, Royal Children's Hospital, Melbourne, VIC, Australia.
S L McGee1] Metabolic Remodelling Laboratory, Metabolic Research Unit, School of Medicine, Deakin University, Geelong, VIC, Australia [2] Division of Cell Signalling and Metabolism, Baker IDI Heart and Diabetes Institute, Melbourne, VIC, Australia.
A J Hannan1] Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, Australia [2] Department of Anatomy and Neuroscience, University of Melbourne, Parkville, VIC, Australia.
L J Gray1] Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC, Australia [2] School of Medicine, Faculty of Health, Deakin University, Geelong, VIC, Australia.
Deakin University · AUUniversity of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Huntington's disease (HD) is a neurodegenerative disorder, involving psychiatric, cognitive and motor symptoms, caused by a CAG-repeat expansion encoding an extended polyglutamine tract in the huntingtin protein. Oxidative stress and excitotoxicity have previously been implicated in the pathogenesis of HD. We hypothesized that N-acetylcysteine (NAC) may reduce both excitotoxicity and oxidative stress through its actions on glutamate reuptake and antioxidant capacity. The R6/1 transgenic mouse model of HD was used to investigate the effects of NAC on HD pathology. It was found that chronic NAC administration delayed the onset and progression of motor deficits in R6/1 mice, while having an antidepressant-like effect on both R6/1 and wild-type mice. A deficit in the astrocytic glutamate transporter protein, GLT-1, was found in R6/1 mice. However, this deficit was not ameliorated by NAC, implying that the therapeutic effect of NAC is not due to rescue of the GLT-1 deficit and associated glutamate-induced excitotoxicity. Assessment of mitochondrial function in the striatum and cortex revealed that R6/1 mice show reduced mitochondrial respiratory capacity specific to the striatum. This deficit was rescued by chronic treatment with NAC. There was a selective increase in markers of oxidative damage in mitochondria, which was rescued by NAC. In conclusion, NAC is able to delay the onset of motor deficits in the R6/1 model of Huntington's disease and it may do so by ameliorating mitochondrial dysfunction. Thus, NAC shows promise as a potential therapeutic agent in HD. Furthermore, our data suggest that NAC may also have broader antidepressant efficacy.

Indexed as

AcetylcysteineAnimalsBehavior, AnimalBrainDisease Models, AnimalDisease ProgressionExcitatory Amino Acid Transporter 2Free Radical ScavengersGaitHuntington DiseaseMiceMice, TransgenicMitochondriaMotor ActivityOrgan SizeOxidative StressAcetylcysteineExcitatory Amino Acid Transporter 2Free Radical ScavengersSlc1a2 protein, mouse

Identifiers

PMID25562842
PMCPMC4312826
OpenAlexW1984521955

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.