Evidence map›Paper›PMID 27445757›Full record

ReviewFrontiers in human neuroscience2016

Corticostriatal Dysfunction in Huntington's Disease: The Basics.

Kendra D Bunner, George V Rebec

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in human neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.8field-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

43 citing papers in PubMed, 61 citations in OpenAlex.

  1. Psychosis in Huntington disease: a short update.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  2. Article
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  9. Advancements in surgical treatments for Huntington disease: From pallidotomy to experimental therapies.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
  10. Pathomechanisms of behavioral abnormalities in Huntington disease: an update.Journal of neural transmission (Vienna, Austria : 1996) · 2024
    Review
  11. Mild cognitive impairment in Huntington's disease: challenges and outlooks.Journal of neural transmission (Vienna, Austria : 1996) · 2024
    Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Revisiting the outcome of adult wild-typeBrain communications · 2023
    Article
  17. HSF1 and Its Role in Huntington's Disease Pathology.Advances in experimental medicine and biology · 2023
    Review
  18. Article
  19. Article
  20. Non-Cell Autonomous and Epigenetic Mechanisms of Huntington's Disease.International journal of molecular sciences · 2021
    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

2 authors at 1 institution in 1 country.

Kendra D BunnerDepartment of Psychological and Brain Sciences, Program in Neuroscience, Indiana University Bloomington, IN, USA.
George V RebecDepartment of Psychological and Brain Sciences, Program in Neuroscience, Indiana University Bloomington, IN, USA.
Indiana University Bloomington · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The main input to the basal ganglia, the corticostriatal pathway, shows some of the earliest signs of neuropathology in Huntington's disease (HD), an inherited neurodegenerative condition that typically strikes in mid-life with progressively deteriorating cognitive, emotional, and motor symptoms. Although an effective treatment remains elusive, research on transgenic animal models has implicated dysregulation of glutamate (Glu), the excitatory amino acid released by corticostriatal neurons, in HD onset. Abnormalities in the control of Glu transmission at the level of postsynaptic receptors and Glu transport proteins play a critical role in the loss of information flow through downstream circuits that set the stage for the HD behavioral phenotype. Parallel but less-well characterized changes in dopamine (DA), a key modulator of Glu activation, ensure further deficits in neuronal communication throughout the basal ganglia. Continued analysis of corticostriatal Glu transmission and its modulation by DA, including analysis at the neurobehavioral level in transgenic models, is likely to be an effective strategy in the pursuit of HD therapeutics.

Indexed as

cortiostriatal circuitrydopamineelectrophysiologyglutamateHuntington’s disease

Identifiers

PMID27445757
PMCPMC4924423
OpenAlexW2468033573

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.