La maladie de Parkinson au Canada (serveur d'exploration)

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Presymptomatic compensation in Parkinson's disease is not dopamine-mediated

Identifieur interne : 002F10 ( Main/Curation ); précédent : 002F09; suivant : 002F11

Presymptomatic compensation in Parkinson's disease is not dopamine-mediated

Auteurs : Erwan Bezard [France] ; Christian E. Gross [France] ; Jonathan M. Brotchie [Canada]

Source :

RBID : Pascal:04-0275228

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English descriptors

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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Pascal:04-0275228

Le document en format XML

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<term>Parkinson disease</term>
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<term>Compensation</term>
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<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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