Reply: Levodopa in the treatment of Parkinson's disease: Current controversies

Olanow, C. Warren; Agid, Yves; Mizuno, Y

doi:10.1002/mds.20426

Cited by 56 publications

(71 citation statements)

References 4 publications

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“…The 6-OHDA ? L-DOPA group comprised eight rats per time point (3,5, and 10 days) while the two control groups (6-OHDA ? Saline; Saline ?…”

Section: Drug Administration and Behavioral Assessmentmentioning

confidence: 99%

“…While perhaps non-toxic to DA neurons, there is little question that early L-DOPA treatment predisposes patients to the onset of disabling abnormal involuntary movements (AIM) [1,5,11]. However, the mechanisms that underlie this complication are poorly understood.…”

Section: Introductionmentioning

confidence: 99%

“…Although L-3,4-dihydroxyphenylalanine (L-DOPA) is highly effective as a treatment for tremor, rigidity and akinesia in Parkinson's disease (PD), its potential toxicity has been the subject of some controversy in recent years [1][2][3][4][5][6]. It is now generally accepted, based on the preponderance of reports, that L-DOPA and its metabolites are not directly toxic to dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc), nor to nigrostriatal fibers [7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

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Striatal Dopaminergic Fiber Recovery After Acute l-DOPA Treatment in 6-Hydroxydopamine (6-OHDA) Lesioned Rats

Fang

Yin

et al. 2010

Cell Biochem Biophys

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In order to examine the acute effects of L: -DOPA treatment following 6-hydroxydopamine (6-OHDA) injection into rat medial forebrain bundle (MFB). Sprague-Dawley rats (n = 48) received either 6-OHDA, via intracranial unilateral injection, into the MFB (experimental group) or saline 0.9% (control group). Administration of L: -DOPA or saline 0.9% began 1 month after the 6-OHDA injection for 10 consecutive days. Within 3 days, an increase in the density of striatal tyrosine hydroxylase (TH) immunoreactive fibers within the striatum, when compared to the control group was observed. There was no difference in the loss of substantia nigra pars compacta (SNpc) dopaminergic (DA) neurons between. The greater density of TH fibers in the striatum following L: -DOPA may be related to recovery of the DA phenotype and/or sprouting of TH axon terminals. Only animals with severe cell loss in the SNpc experienced abnormal involuntary movements (AIMs) or "dyskinesias" in response to L: -DOPA, which did not correlate with striatal TH fiber density, suggesting that induction of TH-positive fibers does not contribute to the occurrence of dyskinesia. The relationship between cell loss, fiber density and AIM to the abundance of markers of microglial activation were also examined. Iba-1, a microglial marker, immunoreactivity was not affected by L: -DOPA treatment, was not correlated with the severity of AIM indicating that microglial activation does not contribute to dyskinetic phenomena.

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“…The 6-OHDA ? L-DOPA group comprised eight rats per time point (3,5, and 10 days) while the two control groups (6-OHDA ? Saline; Saline ?…”

Section: Drug Administration and Behavioral Assessmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Striatal Dopaminergic Fiber Recovery After Acute l-DOPA Treatment in 6-Hydroxydopamine (6-OHDA) Lesioned Rats

Fang

Yin

et al. 2010

Cell Biochem Biophys

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“…Patients receiving the highest dose of L-dopa had significantly more dyskinesia than those receiving placebo. Further clinical trials are underway to study the effects of L-dopa on the progression of PD [33,Class I]. In the meantime, L-dopa remains the most effective therapy for PD and should be introduced when the patient's social, occupational, or self-care functions are sufficiently compromised to warrant treatment with the best available drug for PD.…”

Section: Main Drug Interactionsmentioning

confidence: 99%

Initial treatment of parkinson’s disease

Tarsy

2006

Curr Treat Options Neurol

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“…Existe evidencia respecto a la posibilidad que la aparición de las complicaciones motoras, especialmente las discinesias, dependa parcialmente del modo de administración de la levodopa. Normalmente, la concentración de dopamina estriatal es estable en el día 35 . En portadores de EP, en especial en etapas avanzadas, las concentraciones de levodopa varían de modo significativo en relación con cada toma del fármaco.…”

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Levodopa en la enfermedad de Parkinson: ¿Qué hemos aprendido?

Juri

2006

Rev. méd. Chile

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(Rev Méd Chile 2006; 134: 893-901D esde su introducción en la medicina a inicios de la década de 1960, la L-3,4-dihidroxifenilalanina o levodopa se ha convertido en uno de los fármacos más sorprendentes en neurología. Su capacidad de inducir una mejoría casi milagrosa en sujetos portadores de enfermedad de Parkinson (EP), rápidamente la convirtieron en el medicamento de elección para esta enfermedad 1 . Han pasado casi 50 años desde aquella irrupción de la levodopa en la neurología y continúa siendo el principal fármaco para tratar la EP, al que todos los portadores de esta enfermedad recurrirán durante su evolución.En los últimos años, diversas investigaciones han aportado nuevos conocimientos sobre los mecanismos de acción y la fisiopatología de las complicaciones inducidas por ella. También han surgido nuevas formas de administración y combinaciones terapéu-ticas con levodopa. Todo esto ha revitalizado el debate sobre este compuesto y ha introducido nuevos aspectos a considerar para su uso.El objetivo de esta revisión es repasar estos aspectos y entregar algunas recomendaciones actualizadas para su empleo en la EP en etapa inicial.

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Reply: Levodopa in the treatment of Parkinson's disease: Current controversies

Cited by 56 publications

References 4 publications

Striatal Dopaminergic Fiber Recovery After Acute l-DOPA Treatment in 6-Hydroxydopamine (6-OHDA) Lesioned Rats

Striatal Dopaminergic Fiber Recovery After Acute l-DOPA Treatment in 6-Hydroxydopamine (6-OHDA) Lesioned Rats

Initial treatment of parkinson’s disease

Levodopa en la enfermedad de Parkinson: ¿Qué hemos aprendido?

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