Evidence map›Paper›PMID 25697043›Full record

ReviewProgress in neurobiology2015

Striatal cholinergic dysfunction as a unifying theme in the pathophysiology of dystonia.

K L Eskow Jaunarajs, P Bonsi, M F Chesselet, D G Standaert, A Pisani

Open access · greenAbstract readReview
In one paragraph

Review in Progress in neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers.

0numbers the graph read from it
0cells of the map it votes in
81citing papers in PubMed
9.8field-weighted citation impact, top 1% 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

81 citing papers in PubMed, 158 citations in OpenAlex.

  1. Article
  2. The Second Hit Hypothesis in Animal and Human Dystonia: The Role of Peripheral Nerve Trauma and Spinal Cord Injury.Movement disorders : official journal of the Movement Disorder Society · 2026
    Review
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  13. Suitability of Automated Writing Measures for Clinical Trial Outcome in Writer's Cramp.Movement disorders : official journal of the Movement Disorder Society · 2023
    Article
  14. Review
  15. The pathogenesis of blepharospasm.Frontiers in neurology · 2023
    Review
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21 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

K L Eskow JaunarajsDepartment of Neurology, Center for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, USA.
P BonsiIRCCS Fondazione Santa Lucia, Laboratory of Neurophysiology and Plasticity, Rome, Italy.
M F ChesseletDepartment of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, USA.
D G StandaertDepartment of Neurology, Center for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, USA. Electronic address: dstandaert@uab.edu.
A PisaniIRCCS Fondazione Santa Lucia, Laboratory of Neurophysiology and Plasticity, Rome, Italy; Department of Systems Medicine, University of Rome "Tor Vergata", Italy. Electronic address: pisani@uniroma2.it.
Fondazione Santa Lucia · ITUniversity of Alabama at Birmingham · USUniversity of California, Los Angeles · US

Funding

Torsin Function in DrosiphilaP50NS037409 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI BHIDE, PRADEEP G · 2008 to 2013
$9.2M
Torsin Function in DrosiphilaP01NS037409 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI OZELIUS, LAURIE J. · 1999 to 2007
$8.5M
TorsinA as a key link in receptor-mediated signalingP01NS087997 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI BREAKEFIELD, XANDRA OWENS, OZELIUS, LAURIE J. · 2015 to 2019
$6.4M
Dopamine D1 Receptor in mouse models of primary dystoniaR01NS081282 · NINDS · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI EHRLICH, MICHELLE E, MARTEMYANOV, KIRILL A. · 2013 to 2017
$2.5M
NINDS NIH HHS P01 NS037409NINDS NIH HHS P01 NS087997NINDS NIH HHS P01NS087997NINDS NIH HHS P50 NS037409NINDS NIH HHS P50NS037409NINDS NIH HHS R01 NS081282
6 · The paper itself

Abstract

Dystonia is a movement disorder of both genetic and non-genetic causes, which typically results in twisted posturing due to abnormal muscle contraction. Evidence from dystonia patients and animal models of dystonia indicate a crucial role for the striatal cholinergic system in the pathophysiology of dystonia. In this review, we focus on striatal circuitry and the centrality of the acetylcholine system in the function of the basal ganglia in the control of voluntary movement and ultimately clinical manifestation of movement disorders. We consider the impact of cholinergic interneurons (ChIs) on dopamine-acetylcholine interactions and examine new evidence for impairment of ChIs in dysfunction of the motor systems producing dystonic movements, particularly in animal models. We have observed paradoxical excitation of ChIs in the presence of dopamine D2 receptor agonists and impairment of striatal synaptic plasticity in a mouse model of DYT1 dystonia, which are improved by administration of recently developed M1 receptor antagonists. These findings have been confirmed across multiple animal models of DYT1 dystonia and may represent a common endophenotype by which to investigate dystonia induced by other types of genetic and non-genetic causes and to investigate the potential effectiveness of pharmacotherapeutics and other strategies to improve dystonia.

Indexed as

AcetylcholineAnimalsCorpus StriatumDystonic DisordersHumansInterneuronsAcetylcholineAcetylcholine interneuronsAnimal modelsBasal gangliaDopamineDystoniaStriatum

Identifiers

PMID25697043
PMCPMC4420693
OpenAlexW2006468011

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.