Presymptomatic compensation in Parkinson's disease is not dopamine-mediated.
Identifieur interne : 000F73 ( PubMed/Checkpoint ); précédent : 000F72; suivant : 000F74Presymptomatic compensation in Parkinson's disease is not dopamine-mediated.
Auteurs : Erwan Bezard [France] ; Christian E. Gross ; Jonathan M. BrotchieSource :
- Trends in neurosciences [ 0166-2236 ] ; 2003.
English descriptors
- KwdEn :
- Adaptation, Physiological (physiology), Animals, Basal Ganglia (physiopathology), Disease Progression, Dopamine (metabolism), Enkephalins (genetics), Enkephalins (metabolism), Globus Pallidus (physiopathology), Humans, Models, Neurological, Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Receptors, Dopamine D2 (physiology), Substantia Nigra (physiopathology).
- MESH :
- chemical , genetics : Enkephalins.
- chemical , metabolism : Dopamine, Enkephalins.
- metabolism : Parkinson Disease.
- physiology : Adaptation, Physiological, Receptors, Dopamine D2.
- physiopathology : Basal Ganglia, Globus Pallidus, Parkinson Disease, Substantia Nigra.
- Animals, Disease Progression, Humans, Models, Neurological.
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.
DOI: 10.1016/S0166-2236(03)00038-9
PubMed: 12689773
Affiliations:
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pubmed:12689773Le document en format XML
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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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<Abstract><AbstractText>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.</AbstractText>
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