PD (Parkinson's disease) is characterized by some typical motor features that are caused by striatal dopamine depletion and respond well to dopamine-replacement therapy with L-dopa. Unfortunately, the majority of PD patients treated with L-dopa develop abnormal involuntary movements (dyskinesias) within a few years. The mechanisms underlying the development of LIDs (L-dopa-induced dyskinesias) involve, on one hand, a presynaptic dysregulation of dopamine release and clearance and, on the other hand, an abnormal postsynaptic response to dopamine in the brain. There is a large amount of evidence that these dopamine-dependent mechanisms are modulated by glutamatergic pathways and glutamate receptors. The present article summarizes the pathophysiological role of glutamatergic pathways in LID and reviews pre-clinical and clinical results obtained using pharmacological modulators of different classes and subtypes of glutamate receptors to treat parkinsonian dyskinesias.
Conference Article| March 20 2014
Glutamatergic pathways as a target for the treatment of dyskinesias in Parkinson's disease
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M. Angela Cenci; Glutamatergic pathways as a target for the treatment of dyskinesias in Parkinson's disease. Biochem Soc Trans 1 April 2014; 42 (2): 600–604. doi: https://doi.org/10.1042/BST20140006
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