Evidence map›Paper›PMID 21106706›Full record

ArticleHuman molecular genetics2011

Electroconvulsive shock ameliorates disease processes and extends survival in huntingtin mutant mice.

Mohamed R Mughal, Akanksha Baharani, Srinivasulu Chigurupati, Tae Gen Son, Edmund Chen, Peter Yang, Eitan Okun, Thiruma Arumugam, Sic L Chan, Mark P Mattson

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Human molecular genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.7field-weighted citation impact, top 34% 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

15 citing papers in PubMed, 28 citations in OpenAlex.

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  12. BDNF mediates adaptive brain and body responses to energetic challenges.Trends in endocrinology and metabolism: TEM · 2014
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4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

10 authors at 4 institutions in 2 countries.

Mohamed R MughalLaboratory of Neurosciences, National Institute on Aging Intramural Research Program, Biomedical Research Center, Baltimore, MD 21224, USA.
Akanksha Baharani
Srinivasulu Chigurupati
Tae Gen Son
Edmund Chen
Peter Yang
Eitan Okun
Thiruma Arumugam
Sic L Chan
Mark P Mattson
Institute on Aging · USNational Institute on Aging · USUniversity of Central Florida · USUniversity of Queensland · AU

Funding

Roles of alpha-synuclein in stroke induced brain damageR21NS066265 · NINDS · UNIVERSITY OF CENTRAL FLORIDA · PI CHAN, SIC L · 2009 to 2010
$383k
Intramural NIH HHSNINDS NIH HHS 1R21NS066265-01NINDS NIH HHS R21 NS066265
6 · The paper itself

Abstract

Huntington's disease (HD) is an inherited neurodegenerative disorder caused by expanded polyglutamine repeats in the huntingtin (Htt) protein. Mutant Htt may damage and kill striatal neurons by a mechanism involving reduced production of brain-derived neurotrophic factor (BDNF) and increased oxidative and metabolic stress. Because electroconvulsive shock (ECS) can stimulate the production of BDNF and protect neurons against stress, we determined whether ECS treatment would modify the disease process and provide a therapeutic benefit in a mouse model of HD. ECS (50 mA for 0.2 s) or sham treatment was administered once weekly to male N171-82Q Htt mutant mice beginning at 2 months of age. Endpoints measured included motor function, striatal and cortical pathology, and levels of protein chaperones and BDNF. ECS treatment delayed the onset of motor symptoms and body weight loss and extended the survival of HD mice. Striatal neurodegeneration was attenuated and levels of protein chaperones (Hsp70 and Hsp40) and BDNF were elevated in striatal neurons of ECS-treated compared with sham-treated HD mice. Our findings demonstrate that ECS can increase the resistance of neurons to mutant Htt resulting in improved functional outcome and extended survival. The potential of ECS as an intervention in subjects that inherit the mutant Htt gene merits further consideration.

Indexed as

Disease ProgressionElectroshockAnimalsBrain-Derived Neurotrophic FactorCyclic AMP Response Element-Binding ProteinDisease Models, AnimalGene Expression RegulationHeat-Shock ProteinsHuntington DiseaseMaleMiceMice, TransgenicMutationNerve DegenerationProto-Oncogene Proteins c-aktSerotonin Plasma Membrane Transport ProteinsBrain-Derived Neurotrophic FactorCyclic AMP Response Element-Binding ProteinHeat-Shock ProteinsProto-Oncogene Proteins c-aktSerotonin Plasma Membrane Transport ProteinsSlc6a4 protein, mouse

Identifiers

PMID21106706
PMCPMC3024043
OpenAlexW2161787322

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.