Presymptomatic compensation in Parkinson's disease is not dopamine-mediated
Identifieur interne : 002F10 ( Main/Curation ); précédent : 002F09; suivant : 002F11Presymptomatic compensation in Parkinson's disease is not dopamine-mediated
Auteurs : Erwan Bezard [France] ; Christian E. Gross [France] ; Jonathan M. Brotchie [Canada]Source :
- Trends in neurosciences : (Regular edition) [ 0166-2236 ] ; 2003.
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- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
The symptoms of Parkinson's disease (PD) appear only after substantial degeneration of the dopaminergic neuron system (e.g. an 80% depletion of striatal dopamine) - that is, there is a substantive presymptomatic period of the disease. It is widely believed that dopamine-related compensatory mechanisms are responsible for delaying the appearance of symptoms. Recent advances in understanding the presymptomatic phase of PD have increased our understanding of these dopamine-related compensatory mechanisms and have highlighted the role of non-dopamine-mediated mechanisms both within and outside the basal ganglia. This increased knowledge of plasticity within cortical-basal-ganglia-thalamocortical circuitry as dopaminergic neuron degeneration progresses has implications for understanding plasticity in neural circuits generally and, more specifically, for developing novel therapeutics or presymptomatic diagnostics for PD.
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Compensation</term>
<term>Corpus striatum</term>
<term>Degeneration</term>
<term>Depletion</term>
<term>Dopamine</term>
<term>Dopaminergic neuron</term>
<term>Parkinson disease</term>
<term>Plasticity</term>
<term>Review</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Compensation</term>
<term>Dopamine</term>
<term>Dégénérescence</term>
<term>Neurone dopaminergique</term>
<term>Déplétion</term>
<term>Corps strié</term>
<term>Plasticité</term>
<term>Article synthèse</term>
<term>Parkinson maladie</term>
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<front><div type="abstract" xml:lang="en">The symptoms of Parkinson's disease (PD) appear only after substantial degeneration of the dopaminergic neuron system (e.g. an 80% depletion of striatal dopamine) - that is, there is a substantive presymptomatic period of the disease. It is widely believed that dopamine-related compensatory mechanisms are responsible for delaying the appearance of symptoms. Recent advances in understanding the presymptomatic phase of PD have increased our understanding of these dopamine-related compensatory mechanisms and have highlighted the role of non-dopamine-mediated mechanisms both within and outside the basal ganglia. This increased knowledge of plasticity within cortical-basal-ganglia-thalamocortical circuitry as dopaminergic neuron degeneration progresses has implications for understanding plasticity in neural circuits generally and, more specifically, for developing novel therapeutics or presymptomatic diagnostics for PD.</div>
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