Enhancing Neuroplasticity in the Basal Ganglia: The Role of Exercise in Parkinson’s Disease
Identifieur interne : 002A66 ( Ncbi/Checkpoint ); précédent : 002A65; suivant : 002A67Enhancing Neuroplasticity in the Basal Ganglia: The Role of Exercise in Parkinson’s Disease
Auteurs : Giselle M. Petzinger [États-Unis] ; Beth E. Fisher [États-Unis] ; Jon-Eric Van Leeuwen [États-Unis] ; Marta Vukovic [États-Unis] ; Garnik Akopian [États-Unis] ; Charlie K. Meshul [États-Unis] ; Daniel P. Holschneider [États-Unis] ; Angelo Nacca [États-Unis] ; John P. Walsh [États-Unis] ; Michael W. Jakowec [États-Unis]Source :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2010.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Dopamine.
- epidemiology : Parkinson Disease.
- pathology : Basal Ganglia, Parkinson Disease.
- physiology : Basal Ganglia, Neuronal Plasticity.
- rehabilitation : Parkinson Disease.
- Exercise, Humans, Sensitivity and Specificity.
Abstract
Epidemiological and clinical trials have suggested that exercise is beneficial for patients with Parkinson’s disease (PD). However, the underlying mechanisms and potential for disease modification are currently unknown. This review presents current findings from our laboratories in patients with PD and animal models. The data indicate that alterations in both dopaminergic and glutamatergic neurotransmission, induced by activity-dependent (exercise) processes, may mitigate the cortically driven hyper-excitability in the basal ganglia normally observed in the parkinsonian state. These insights have potential to identify novel therapeutic treatments capable of reversing or delaying disease progression in PD.
Url:
DOI: 10.1002/mds.22782
PubMed: 20187247
PubMed Central: 4111643
Affiliations:
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PMC:4111643Le document en format XML
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<author><name sortKey="Jakowec, Michael W" sort="Jakowec, Michael W" uniqKey="Jakowec M" first="Michael W." last="Jakowec">Michael W. Jakowec</name>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Basal Ganglia (pathology)</term>
<term>Basal Ganglia (physiology)</term>
<term>Dopamine (metabolism)</term>
<term>Exercise</term>
<term>Humans</term>
<term>Neuronal Plasticity (physiology)</term>
<term>Parkinson Disease (epidemiology)</term>
<term>Parkinson Disease (pathology)</term>
<term>Parkinson Disease (rehabilitation)</term>
<term>Sensitivity and Specificity</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term>
</keywords>
<keywords scheme="MESH" qualifier="epidemiology" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Basal Ganglia</term>
<term>Parkinson Disease</term>
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<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Basal Ganglia</term>
<term>Neuronal Plasticity</term>
</keywords>
<keywords scheme="MESH" qualifier="rehabilitation" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
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<front><div type="abstract" xml:lang="en"><p id="P1">Epidemiological and clinical trials have suggested that exercise is beneficial for patients with Parkinson’s disease (PD). However, the underlying mechanisms and potential for disease modification are currently unknown. This review presents current findings from our laboratories in patients with PD and animal models. The data indicate that alterations in both dopaminergic and glutamatergic neurotransmission, induced by activity-dependent (exercise) processes, may mitigate the cortically driven hyper-excitability in the basal ganglia normally observed in the parkinsonian state. These insights have potential to identify novel therapeutic treatments capable of reversing or delaying disease progression in PD.</p>
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<name sortKey="Petzinger, Giselle M" sort="Petzinger, Giselle M" uniqKey="Petzinger G" first="Giselle M." last="Petzinger">Giselle M. Petzinger</name>
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