Evidence map›Paper›PMID 25703232›Full record

ArticleRedox biology2015

Neonatal iron supplementation potentiates oxidative stress, energetic dysfunction and neurodegeneration in the R6/2 mouse model of Huntington's disease.

Kiersten L Berggren, Jianfang Chen, Julia Fox, Jonathan Miller, Lindsay Dodds, Bryan Dugas, Liset Vargas, Amber Lothian, Erin McAllum, Irene Volitakis and 3 more

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

Article in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 17% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Ferroptosis: underlying mechanisms and involvement in neurodegenerative diseases.Apoptosis : an international journal on programmed cell death · 2024
    Review
  11. Review
  12. Review
  13. Oral administration of live combinedFrontiers in microbiology · 2022
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review
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

13 authors at 2 institutions in 2 countries.

Kiersten L BerggrenDepartment of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, Laramie, WY 82070, USA. Electronic address: kberggre@uwyo.edu.
Jianfang ChenDepartment of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, Laramie, WY 82070, USA; Neuroscience Graduate Program, University of Wyoming, 1174 Snowy Range Road, Laramie, WY 82070, USA. Electronic address: chenjianfang11@gmail.com.
Julia FoxDepartment of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, Laramie, WY 82070, USA. Electronic address: jfox8@uwyo.edu.
Jonathan MillerDepartment of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, Laramie, WY 82070, USA. Electronic address: jmill129@uwyo.edu.
Lindsay DoddsDepartment of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, Laramie, WY 82070, USA. Electronic address: ldodds917@gmail.com.
Bryan DugasDepartment of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, Laramie, WY 82070, USA. Electronic address: dugas@uw.edu.
Liset VargasDepartment of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, Laramie, WY 82070, USA. Electronic address: lvargas1@uwyo.edu.
Amber LothianFlorey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria 3010, Australia.
Erin McAllumFlorey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria 3010, Australia.
Irene VolitakisFlorey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria 3010, Australia. Electronic address: irene.volitakis@florey.edu.au.
Blaine RobertsFlorey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria 3010, Australia. Electronic address: blaine.roberts@florey.edu.au.
Ashley I BushFlorey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria 3010, Australia. Electronic address: ashleyib@unimelb.edu.au.
Jonathan H FoxDepartment of Veterinary Sciences, University of Wyoming, 1174 Snowy Range Road, Laramie, WY 82070, USA; Neuroscience Graduate Program, University of Wyoming, 1174 Snowy Range Road, Laramie, WY 82070, USA. Electronic address: jfox7@uwyo.edu.
University of Wyoming · USThe University of Melbourne · AU

Funding

Defining the role of brain iron dysregulation in Huntington's diseaseR01NS079450 · NINDS · UNIVERSITY OF WYOMING · PI FOX, JONATHAN H · 2012 to 2015
$1.2M
NINDS NIH HHS R01 NS079450NINDS NIH HHS R01NS079450
6 · The paper itself

Abstract

Huntington's disease (HD) is a progressive neurodegenerative disorder caused by a CAG repeat expansion that encodes a polyglutamine tract in huntingtin (htt) protein. Dysregulation of brain iron homeostasis, oxidative stress and neurodegeneration are consistent features of the HD phenotype. Therefore, environmental factors that exacerbate oxidative stress and iron dysregulation may potentiate HD. Iron supplementation in the human population is common during infant and adult-life stages. In this study, iron supplementation in neonatal HD mice resulted in deterioration of spontaneous motor running activity, elevated levels of brain lactate and oxidized glutathione consistent with increased energetic dysfunction and oxidative stress, and increased striatal and motor cortical neuronal atrophy, collectively demonstrating potentiation of the disease phenotype. Oxidative stress, energetic, and anatomic markers of degeneration were not affected in wild-type littermate iron-supplemented mice. Further, there was no effect of elevated iron intake on disease outcomes in adult HD mice. We have demonstrated an interaction between the mutant huntingtin gene and iron supplementation in neonatal HD mice. Findings indicate that elevated neonatal iron intake potentiates mouse HD and promotes oxidative stress and energetic dysfunction in brain. Neonatal-infant dietary iron intake level may be an environmental modifier of human HD.

Indexed as

AnimalsAnimals, NewbornBehavior, AnimalCorpus StriatumDietary SupplementsDisease Models, AnimalEnergy MetabolismFemaleGene ExpressionGlutathione DisulfideHumansHuntington DiseaseIron CompoundsMiceMice, TransgenicMotor CortexGlutathione DisulfideIron Compoundsiron pentacarbonylSerotonin Plasma Membrane Transport ProteinsSlc6a4 protein, mouseGene environment interactionHuntington’sIronNeurodegenerationOxidative stressStereology

Identifiers

PMID25703232
PMCPMC4348428
OpenAlexW1976216153

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.