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Glutamatergic pathways as a target for the treatment of dyskinesias in Parkinson's disease.

Cenci Nilsson, Angela LU (2014) In Biochemical Society Transactions 42(2). p.600-604
Abstract
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... (More)
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. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Biochemical Society Transactions
volume
42
issue
2
pages
600 - 604
publisher
Biochemical Society
external identifiers
  • pmid:24646284
  • wos:000333658900061
  • scopus:84896962028
ISSN
0300-5127
DOI
10.1042/BST20140006
language
English
LU publication?
yes
id
23ae2806-879c-46e4-903f-c6ee984ecd6c (old id 4382977)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24646284?dopt=Abstract
date added to LUP
2014-04-03 20:21:16
date last changed
2017-05-14 04:23:36
@article{23ae2806-879c-46e4-903f-c6ee984ecd6c,
  abstract     = {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.},
  author       = {Cenci Nilsson, Angela},
  issn         = {0300-5127},
  language     = {eng},
  number       = {2},
  pages        = {600--604},
  publisher    = {Biochemical Society},
  series       = {Biochemical Society Transactions},
  title        = {Glutamatergic pathways as a target for the treatment of dyskinesias in Parkinson's disease.},
  url          = {http://dx.doi.org/10.1042/BST20140006},
  volume       = {42},
  year         = {2014},
}