Abstract |
Levodopa-induced dyskinesias (LID) represent a substantial barrier to effective symptomatic management of Parkinson's disease, but current treatment options for this debilitating side effect are limited, despite an increasing understanding of their pathophysiology from animal models. Increasing evidence suggests that serotonin neurons have a pivotal role in the induction and maintenance of dyskinesias, and provide a promising target for anti-dyskinetic therapies. Here, we review the evidence for serotonergic involvement in dyskinesias from animal and human data, and highlight some of the translational gaps which may explain why the success of serotonin autoreceptor agonists as anti-dyskinetic agents in experimental models has failed to be replicated in clinical trials.
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Authors | Perdita A Cheshire, David R Williams |
Journal | Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia
(J Clin Neurosci)
Vol. 19
Issue 3
Pg. 343-8
(Mar 2012)
ISSN: 1532-2653 [Electronic] Scotland |
PMID | 22249009
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Copyright | Copyright © 2011 Elsevier Ltd. All rights reserved. |
Chemical References |
- Anti-Dyskinesia Agents
- Antiparkinson Agents
- Dopamine Agents
- Serotonin
- Levodopa
- Dopamine
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Topics |
- Animals
- Anti-Dyskinesia Agents
(therapeutic use)
- Antiparkinson Agents
(adverse effects)
- Dopamine
(physiology)
- Dopamine Agents
(adverse effects, therapeutic use)
- Dyskinesia, Drug-Induced
(physiopathology)
- Humans
- Levodopa
(adverse effects, pharmacokinetics)
- Neurons
(physiology)
- Parkinson Disease
(complications, drug therapy)
- Serotonin
(physiology)
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