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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4382977
- author
- Cenci Nilsson, Angela
LU
- organization
- publishing date
- 2014
- 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
- pmid:24646284
- 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
- 2016-04-04 08:05:10
- date last changed
- 2022-05-16 20:52:08
@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}},
doi = {{10.1042/BST20140006}},
volume = {{42}},
year = {{2014}},
}