Document Detail


Some molecular mechanisms of dopaminergic and glutamatergic dysfunctioning in Parkinson's disease.
MedLine Citation:
PMID:  23196983     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Parkinson's disease (PD) is a chronic progressive neurodegenerative disorder with a considerable socioeconomic burden. The pathomechanism of PD clearly involves the synergistic interaction of dopaminergic and glutamatergic dysfunctioning, including maladaptive corticostriatal synaptoplasticity. Most of the available treatment options have the aim of restoration of the physiological dopaminergic activity. Currently, the most widely used treatment is L-3,4-dihydroxyphenylalanine (L-DOPA), which leads to the best symptomatic relief in PD. However, the long-term use of L-DOPA results in abnormal involuntary movements in almost all cases, the development of these dyskinetic movements also involving maladaptive corticostriatal synaptoplasticity. Perhaps chronic L-DOPA treatment has neurotoxic effects as well, but it has not yet been proved in clinical studies. Another important group of dopamine replacement therapy (DRT)-related side-effects consists of disinhibitory psychopathologies. Recent studies revealed that genetic polymorphisms affecting certain dopaminergic and glutamatergic receptors serve as independent risk factors for the development of these pathological conditions in PD patients. The available scientific data demonstrate that alterations in the kynurenine pathway of the tryptophan metabolism can be observed in PD and these alterations may contribute to the disease pathogenesis and to the occurrence of DRT-related side-effects. Therapeutic strategies that target the restoration of the kynurenine metabolism could therefore hold promise.
Authors:
Dénes Zádori; Levente Szalárdy; József Toldi; Ferenc Fülöp; Péter Klivényi; László Vécsei
Related Documents :
14552023 - Pemphigus: update for the general practitioner.
8763423 - Keratinocytes express dipeptidyl-peptidase iv (cd26) in benign and malignant skin disea...
24834283 - Metabonomics exposes metabolic biomarkers of crohn's disease by (1)hnmr.
Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-11-30
Journal Detail:
Title:  Journal of neural transmission (Vienna, Austria : 1996)     Volume:  -     ISSN:  1435-1463     ISO Abbreviation:  J Neural Transm     Publication Date:  2012 Nov 
Date Detail:
Created Date:  2012-11-30     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9702341     Medline TA:  J Neural Transm     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
Department of Neurology, Albert Szent-Györgyi Clinical Centre, University of Szeged, Semmelweis u. 6, 6725, Szeged, Hungary.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Switch from selegiline to rasagiline is beneficial in patients with Parkinson's disease.
Next Document:  Enhanced root colonization and biocontrol activity of Bacillus amyloliquefaciens SQR9 by abrB gene d...