Evidence map›Paper›PMID 24336051›Full record

ArticleNature communications2013

A failure in energy metabolism and antioxidant uptake precede symptoms of Huntington's disease in mice.

Aníbal I Acuña, Magdalena Esparza, Carlos Kramm, Felipe A Beltrán, Alejandra V Parra, Carlos Cepeda, Carlos A Toro, René L Vidal, Claudio Hetz, Ilona I Concha and 3 more

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

52 citing papers in PubMed, 110 citations in OpenAlex.

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  20. (Ascorb)ing Pb Neurotoxicity in the Developing Brain.Antioxidants (Basel, Switzerland) · 2020
    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 4 institutions in 2 countries.

Aníbal I Acuña1] Instituto de Bioquímica y Microbiología, Facultad de Ciencias, Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile [2] Centro de Investigación Sur-Austral en Enfermedades del Sistema Nervioso (CISNe), Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile [3] Escuela de Graduados, Facultad de Ciencias, Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile [4].
Magdalena Esparza1] Instituto de Bioquímica y Microbiología, Facultad de Ciencias, Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile [2] Centro de Investigación Sur-Austral en Enfermedades del Sistema Nervioso (CISNe), Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile [3].
Carlos Kramm1] Instituto de Bioquímica y Microbiología, Facultad de Ciencias, Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile [2] Centro de Investigación Sur-Austral en Enfermedades del Sistema Nervioso (CISNe), Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile [3].
Felipe A Beltrán1] Instituto de Bioquímica y Microbiología, Facultad de Ciencias, Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile [2] Centro de Investigación Sur-Austral en Enfermedades del Sistema Nervioso (CISNe), Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile [3] Escuela de Graduados, Facultad de Ciencias, Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile.
Alejandra V Parra1] Instituto de Bioquímica y Microbiología, Facultad de Ciencias, Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile [2] Centro de Investigación Sur-Austral en Enfermedades del Sistema Nervioso (CISNe), Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile.
Carlos CepedaIntellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, Brain Research Institute, The David Geffen School of Medicine, 760 Westwood Plaza, University of California Los Angeles, Los Angeles, California 90095-1759, USA.
Carlos A Toro1] Escuela de Graduados, Facultad de Ciencias, Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile [2] Instituto de Fisiología, Facultad de Medicina, Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile.
René L VidalInstituto de Ciencias Biomédicas, Universidad de Chile, Avda, Independencia 1027, Santiago, Chile.
Claudio HetzNeurounion Biomedical Foundation, Independencia 1027, Santiago, Chile.
Ilona I ConchaInstituto de Bioquímica y Microbiología, Facultad de Ciencias, Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile.
Sebastián Brauchi1] Centro de Investigación Sur-Austral en Enfermedades del Sistema Nervioso (CISNe), Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile [2] Instituto de Fisiología, Facultad de Medicina, Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile.
Michael S LevineIntellectual and Developmental Disabilities Research Center, Semel Institute for Neuroscience and Human Behavior, Brain Research Institute, The David Geffen School of Medicine, 760 Westwood Plaza, University of California Los Angeles, Los Angeles, California 90095-1759, USA.
Maite A Castro1] Instituto de Bioquímica y Microbiología, Facultad de Ciencias, Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile [2] Centro de Investigación Sur-Austral en Enfermedades del Sistema Nervioso (CISNe), Universidad Austral de Chile, Campus Isla Teja s/n, Valdivia, 5090000 Chile.
Austral University of Chile · CLUniversity of California, Los Angeles · USNeurounion Biomedical Foundation · CLUniversity of Chile · CL

Funding

Transgenic Mouse Models of Huntington's DiseaseR01NS041574 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LEVINE, MICHAEL S. · 2002 to 2016
$5.4M
NINDS NIH HHS R01 NS041574
6 · The paper itself

Abstract

Huntington's disease has been associated with a failure in energy metabolism and oxidative damage. Ascorbic acid is a powerful antioxidant highly concentrated in the brain where it acts as a messenger, modulating neuronal metabolism. Using an electrophysiological approach in R6/2 HD slices, we observe an abnormal ascorbic acid flux from astrocytes to neurons, which is responsible for alterations in neuronal metabolic substrate preferences. Here using striatal neurons derived from knock-in mice expressing mutant huntingtin (STHdhQ cells), we study ascorbic acid transport. When extracellular ascorbic acid concentration increases, as occurs during synaptic activity, ascorbic acid transporter 2 (SVCT2) translocates to the plasma membrane, ensuring optimal ascorbic acid uptake for neurons. In contrast, SVCT2 from cells that mimic HD symptoms (dubbed HD cells) fails to reach the plasma membrane under the same conditions. We reason that an early impairment of ascorbic acid uptake in HD neurons could lead to early metabolic failure promoting neuronal death.

Indexed as

Energy MetabolismAnimalsAscorbic AcidAstrocytesCell LineCell MembraneDisease Models, AnimalFemaleHuntingtin ProteinHuntington DiseaseMaleMiceMice, TransgenicNerve Tissue ProteinsNeurogliaNeuronsAscorbic AcidHTT protein, humanHuntingtin ProteinNerve Tissue ProteinsSlc23a2 protein, mouseSodium-Coupled Vitamin C Transporters

Identifiers

PMID24336051
PMCPMC3905737
OpenAlexW1989179698

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.