Evidence map›Paper›PMID 28831764›Full record

ArticleEJNMMI research2017

Motor impairment and compensation in a hemiparkinsonian rat model: correlation between dopamine depletion severity, cerebral metabolism and gait patterns.

Elena Kordys, Nadine Apetz, Katharina Schneider, Eilidh Duncan, Beatriz Büschbell, Cathrin Rohleder, Michael Sué, Alexander Drzezga, Bernd Neumaier, Lars Timmermann and 1 more

Open access · goldAbstract read
In one paragraph

Article in EJNMMI research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 23 citations in OpenAlex.

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  10. Evaluation of exercise-induced modulation of glial activation and dopaminergic damage in a rat model of Parkinson's disease using [Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
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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

11 authors at 5 institutions in 1 country.

Elena KordysInstitute of Radiochemistry and Experimental Molecular Imaging, University Hospital of Cologne, Kerpener Str. 62, 50937, Köln, Germany.
Nadine ApetzInstitute of Radiochemistry and Experimental Molecular Imaging, University Hospital of Cologne, Kerpener Str. 62, 50937, Köln, Germany.
Katharina SchneiderInstitute of Radiochemistry and Experimental Molecular Imaging, University Hospital of Cologne, Kerpener Str. 62, 50937, Köln, Germany.
Eilidh DuncanInstitute of Radiochemistry and Experimental Molecular Imaging, University Hospital of Cologne, Kerpener Str. 62, 50937, Köln, Germany.
Beatriz BüschbellInstitute of Radiochemistry and Experimental Molecular Imaging, University Hospital of Cologne, Kerpener Str. 62, 50937, Köln, Germany.
Cathrin RohlederInstitute of Radiochemistry and Experimental Molecular Imaging, University Hospital of Cologne, Kerpener Str. 62, 50937, Köln, Germany.
Michael SuéMax-Planck Institute of Metabolism Research, Gleueler Str. 50, 50931, Köln, Germany.
Alexander DrzezgaDepartment of Nuclear Medicine, University Hospital of Cologne, Kerpener Str. 62, 50937, Köln, Germany.
Bernd NeumaierInstitute of Radiochemistry and Experimental Molecular Imaging, University Hospital of Cologne, Kerpener Str. 62, 50937, Köln, Germany.
Lars TimmermannDepartment of Neurology, University Hospital of Cologne, Kerpener Str. 62, 50937, Köln, Germany.
Heike EndepolsInstitute of Radiochemistry and Experimental Molecular Imaging, University Hospital of Cologne, Kerpener Str. 62, 50937, Köln, Germany. heike.endepols@uk-koeln.de.ORCID http://orcid.org/0000-0002-6166-4818
University Hospital Cologne · DEForschungszentrum Jülich · DEHeidelberg University · DEMax Planck Institute for Metabolism Research · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn Parkinson's disease (PD), cerebral dopamine depletion is associated with PD subtype-specific metabolic patterns of hypo- and hypermetabolism. It has been hypothesised that hypometabolism reflects impairment, while hypermetabolism may indicate compensatory activity. In order to associate metabolic patterns with pathophysiological and compensatory mechanisms, we combined resting state [

resultsWe found unilateral nigro-striatal dopaminergic loss to decrease swing speed of the contralesional forelimb and stride length of all paws in association with depletion severity. Depletion severity was found to correlate with compensatory changes such as increased stance time of the other three paws and diagonal weight shift to the ipsilesional hind paw. [

conclusionsOur results indicate that ipsilesional hypo- and contralesional hypermetabolism contribute to both motor impairment and compensation. This is the first time when energy metabolism, dopamine depletion and gait analysis were combined in a hemiparkinsonian model. By experimentally increasing or decreasing compensational brain activity, its potential and limits can be further investigated.

Indexed as

Brain metabolismDopamineGait analysisHemiparkinsonian rat modelPositron emission tomography

Identifiers

PMID28831764
PMCPMC5567589
OpenAlexW2746307765

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.