Evidence map›Paper›PMID 20406248›Full record

ReviewCNS neuroscience & therapeutics2010

Dopamine and glutamate in Huntington's disease: A balancing act.

Véronique M André, Carlos Cepeda, Michael S Levine

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in CNS neuroscience & therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
5.6field-weighted citation impact, top 3% 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

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 182 citations in OpenAlex.

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  17. Pathological cell assembly dynamics in a striatal MSN network model.Frontiers in computational neuroscience · 2024
    Article
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18 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

3 authors at 2 institutions in 1 country.

Véronique M AndréIntellectual and Developmental Disabilities Research Center, Semel Institute, Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, USA. vandre@mednet.ucla.edu <vandre@mednet.ucla.edu>
Carlos Cepeda
Michael S Levine
University of California, Los Angeles · USNeurobehavioral Systems · US

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 (HD) is caused by a CAG repeat expansion in exon 1 of the HD gene resulting in a long polyglutamine tract in the N-terminus of the protein huntingtin. Patients carrying the mutation display chorea in early stages followed by akinesia and sometimes dystonia in late stages. Other major symptoms include depression, anxiety, irritability or aggressive behavior, and apathy. Although many neuronal systems are affected, dysfunction and subsequent neurodegeneration in the basal ganglia and cortex are the most apparent pathologies. In HD, the primary hypothesis has been that there is an initial overactivity of glutamate neurotransmission that produces excitotoxicity followed by a series of complex changes that are different in the striatum and in the cortex. This review will focus on evidence for alterations in dopamine (DA)-glutamate interactions in HD, concentrating on the striatum and cortex. The most recent evidence points to decreases in DA and glutamate neurotransmission as the HD phenotype develops. However, there is some evidence for increased DA and glutamate functions that could be responsible for some of the early HD phenotype. Significant evidence indicates that glutamate and dopamine neurotransmission is affected in HD, compromising the fine balance in which DA modulates glutamate-induced excitation in the basal ganglia and cortex. Restoring the balance between glutamate and dopamine could be helpful to treat HD symptoms.

Indexed as

AnimalsCerebral CortexCorpus StriatumDisease Models, AnimalDopamineGlutamic AcidHumansHuntington DiseaseMiceRatsDopamineGlutamic Acid

Identifiers

PMID20406248
PMCPMC3118459
OpenAlexW1507443798

What OpenQuestion holds

Textmetadata
LicenceTDM
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.