Serotonin and Parkinson's disease: On movement, mood, and madness.
Identifieur interne : 001D25 ( PubMed/Curation ); précédent : 001D24; suivant : 001D26Serotonin and Parkinson's disease: On movement, mood, and madness.
Auteurs : Susan H. Fox [Canada] ; Rosalind Chuang ; Jonathan M. BrotchieSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2009.
English descriptors
- KwdEn :
- Affect (physiology), Animals, Dyskinesia, Drug-Induced, Humans, Mental Disorders (complications), Mental Disorders (metabolism), Movement (physiology), Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Serotonin (metabolism), Serotonin Agents (adverse effects), Serotonin Agents (therapeutic use).
- MESH :
- chemical , adverse effects : Serotonin Agents.
- chemical , metabolism : Serotonin.
- complications : Mental Disorders.
- drug therapy : Parkinson Disease.
- metabolism : Mental Disorders, Parkinson Disease.
- physiology : Affect, Movement.
- physiopathology : Parkinson Disease.
- chemical , therapeutic use : Serotonin Agents.
- Animals, Dyskinesia, Drug-Induced, Humans.
Abstract
An appreciation of the multiple roles that serotonin (5-HT) may play in Parkinson's disease (PD) has increased in recent years. Early pathological studies in PD demonstrated nonselective reductions of 5-HT in brain tissue but little correlation to comorbidities such as dyskinesia and mood disturbance. This, combined with treatment failures using serotonergic drugs in comparison to levodopa, meant the field was largely neglected until recently. The multitude of subtypes of 5-HT receptors in the brain and an increased understanding of the potential function 5-HT may play in modulating other neurotransmitter systems, including dopamine, GABA, and glutamate, have meant an expansion in efforts to develop potential serotonergic drugs for both motor and nonmotor symptoms in PD. However, several unanswered questions remain, and future studies need to focus on correlating changes in 5-HT neurotransmission in both pathological and in vivo imaging studies with a full clinical phenotype.
DOI: 10.1002/mds.22473
PubMed: 19412960
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pubmed:19412960Le document en format XML
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<author><name sortKey="Fox, Susan H" sort="Fox, Susan H" uniqKey="Fox S" first="Susan H" last="Fox">Susan H. Fox</name>
<affiliation wicri:level="1"><nlm:affiliation>Movement Disorders Clinic, University of Toronto, Toronto Western Hospital, Ontario, Canada. sfox@uhnresearch.ca</nlm:affiliation>
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<author><name sortKey="Chuang, Rosalind" sort="Chuang, Rosalind" uniqKey="Chuang R" first="Rosalind" last="Chuang">Rosalind Chuang</name>
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<front><div type="abstract" xml:lang="en">An appreciation of the multiple roles that serotonin (5-HT) may play in Parkinson's disease (PD) has increased in recent years. Early pathological studies in PD demonstrated nonselective reductions of 5-HT in brain tissue but little correlation to comorbidities such as dyskinesia and mood disturbance. This, combined with treatment failures using serotonergic drugs in comparison to levodopa, meant the field was largely neglected until recently. The multitude of subtypes of 5-HT receptors in the brain and an increased understanding of the potential function 5-HT may play in modulating other neurotransmitter systems, including dopamine, GABA, and glutamate, have meant an expansion in efforts to develop potential serotonergic drugs for both motor and nonmotor symptoms in PD. However, several unanswered questions remain, and future studies need to focus on correlating changes in 5-HT neurotransmission in both pathological and in vivo imaging studies with a full clinical phenotype.</div>
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