CommentaryAdverse reactions to levodopa: drug toxicity or progression of disease?
References (8)
- et al.
Does long term aggravation of Parkinson's disease result from non-dopaminergic lesions?
Neurology
(1987) Is Ievodopa toxic?
Neurology
(1996)- et al.
Multi-center study of Parkinson's mortality with early versus late dopa treatment
Ann Neurol
(1987) - et al.
Autopsy findings in parkinsonism following treatment with levodopa
Neurology
(1972)
Cited by (40)
Ferroptosis and its potential role in the physiopathology of Parkinson's Disease
2021, Progress in NeurobiologyCitation Excerpt :Disparity in the potential neuroprotective actions of this drug may arise from L-DOPA’s interference with the striatal presynaptic dopamine transporter; standardly used as a reporter for nigro-striatal degeneration by DAT SPECT in clinical trials (Fahn et al., 2004; Fahn, 2005). The powerful symptomatic action and short half-life of L-DOPA also weakens its clinical use with motor complications such as “wearing off” and dyskinesia occurring 4-6 years after chronic use, depending on disease severity (Agid et al., 1998; Agid et al., 2002; Tran et al., 2018). To delay the onset of such complications, dopamine agonists, monoamine oxidase-B (MAO-B) inhibitors or catechol-O-methyltransferase (COMT) inhibitors are prescribed as concomitant therapies.
Glial activation is associated with l-DOPA induced dyskinesia and blocked by a nitric oxide synthase inhibitor in a rat model of Parkinson's disease
2015, Neurobiology of DiseaseCitation Excerpt :The issue of l-DOPA toxicity has been raised in previous literature when discussing potential mechanisms of PD progression and development of dyskinesia and motor fluctuations, which are not observed in untreated patients. However, neither clinical (Agid et al., 1998; Jenner and Brin, 1998) nor experimental studies (Lindgren et al., 2007; Murer et al., 1998) have been able to prove that l-DOPA accelerate DA cell loss in PD, nor that is causes neurodegeneration in the Str. However, there is evidence of ongoing neuroinflammation in the brain of PD patients, and it remains to be established whether l-DOPA contributes to this process, at least in patients affected by l-DOPA-induced dyskinesia.
Intermittent l-DOPA treatment differentially alters synaptotagmin 4 and 7 gene expression in the striatum of hemiparkinsonian rats
2008, Brain ResearchCitation Excerpt :The antiparkinsonic l-DOPA therapy in Parkinson's disease (PD) still remains the best symptomatic treatment for motor deficits that are caused by the functional disturbance of the basal ganglia networks after the degeneration of dopaminergic neurons (Agid et al., 1998; Albin et al., 1989).
Rationale for and use of NMDA receptor antagonists in Parkinson's disease
2004, Pharmacology and Therapeutics