Evidence map›Paper›PMID 31226324›Full record

ReviewBrain research2019

Voluntary exercise delays progressive deterioration of markers of metabolism and behavior in a mouse model of Parkinson's disease.

Jing-Huei Lai, Kai-Yun Chen, John Chung-Che Wu, Lars Olson, Stefan Brené, Chi-Zong Huang, Yen-Hua Chen, Shuo-Jhen Kang, Kuo-Hsing Ma, Barry J Hoffer and 2 more

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

Review in Brain research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 2 pooled it
2.2field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 25 citations in OpenAlex.

  1. Pooled it
  2. Effect of Exercise on Parkinson's Disease Tremor: A Meta-analysis Study.Tremor and other hyperkinetic movements (New York, N.Y.) · 2021
    Pooled it
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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

12 authors at 6 institutions in 3 countries.

Jing-Huei LaiCore Laboratory of Neuroscience, Office of R&D, Taipei Medical University, Taipei, Taiwan; Center for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei, Taiwan.
Kai-Yun ChenCenter for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei, Taiwan; Graduate Institute of Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
John Chung-Che WuCenter for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei, Taiwan; Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Department of Neurosurgery, Taipei Medical University Hospital, Taipei, Taiwan.
Lars OlsonDepartment of Neuroscience, Karolinska Institutet, SE-171 77 Stockholm, Sweden.
Stefan BrenéDepartment of Neuroscience, Karolinska Institutet, SE-171 77 Stockholm, Sweden.
Chi-Zong HuangCenter for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei, Taiwan; Graduate Institute of Neural Regenerative Medicine, College of Medical Science and Technology, Taipei Medical University, Taipei, Taiwan.
Yen-Hua ChenCenter for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei, Taiwan; Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Shuo-Jhen KangCenter for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei, Taiwan; Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.
Kuo-Hsing MaDepartment of Biology and Anatomy, National Defense Medical Center, Taipei, Taiwan.
Barry J HofferDepartment of Neurosurgery, Case Western Reserve University, School of Medicine, Cleveland, OH, USA.
Tsung-Hsun HsiehDepartment of Physical Therapy and Graduate Institute of Rehabilitation Science, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
Yung-Hsiao ChiangCore Laboratory of Neuroscience, Office of R&D, Taipei Medical University, Taipei, Taiwan; Center for Neurotrauma and Neuroregeneration, Taipei Medical University, Taipei, Taiwan; Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Department of Neurosurgery, Taipei Medical University Hospital, Taipei, Taiwan. Electronic address: ychiang@tmu.edu.tw.
Taipei Medical University · TWKarolinska Institutet · SETaipei Medical University Hospital · TWChang Gung University · TWNational Defense Medical Center · TWUniversity School · US

Funding

Repositioning Gliptins for Parkinson's Disease TreatmentR01NS094152 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI HOFFER, BARRY J, LUO, YU · 2015 to 2018
$1.1M
NINDS NIH HHS R01 NS094152
6 · The paper itself

Abstract

Although a good deal is known about the genetics and pathophysiology of Parkinson's disease (PD), and information is emerging about its cause, there are no pharmacological treatments shown to have a significant, sustained capacity to prevent or attenuate the ongoing neurodegenerative processes. However, there is accumulating clinical results to suggest that physical exercise is such a treatment, and studies of animal models of the dopamine (DA) deficiency associated with the motor symptoms of PD further support this hypothesis. Exercise is a non-pharmacological, economically practical, and sustainable intervention with little or no risk and with significant additional health benefits. In this study, we investigated the long-term effects of voluntary exercise on motor behavior and brain biochemistry in the transgenic MitoPark mouse PD model with progressive degeneration of the DA systems caused by DAT-driven deletion of the mitochondrial transcription factor TFAM in DA neurons. We found that voluntary exercise markedly improved behavioral function, including overall motor activity, narrow beam walking, and rotarod performance. There was also improvement of biochemical markers of nigrostriatal DA input. This was manifested by increased levels of DA measured by HPLC, and of the DA membrane transporter measured by PET. Moreover, exercise increased oxygen consumption and, by inference, ATP production via oxidative phosphorylation. Thus, exercise augmented aerobic mitochondrial oxidative metabolism vs glycolysis in the nigrostriatal system. We conclude that there are clear-cut physiological mechanisms for beneficial effects of exercise in PD.

Indexed as

AnimalsBiomarkersCorpus StriatumDisease Models, AnimalDNA-Binding ProteinsDopamineDopamine Plasma Membrane Transport ProteinsDopaminergic NeuronsMaleMiceMice, Inbred C57BLMice, TransgenicMitochondriaMotor ActivityParkinson DiseasePhysical ExertionBiomarkersDNA-Binding ProteinsDopamineDopamine Plasma Membrane Transport ProteinsTranscription FactorsTyrosine 3-MonooxygenaseDopamineExerciseMitochondriaParkinson’s diseasePET

Identifiers

PMID31226324
PMCPMC6702069
OpenAlexW2951626740

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.