L-Dopa Therapy Combined with Peripheral Decarboxylase Inhibitor (MK-486) in Parkinsonism

Ohmoto, Takashi; Kishikawa, Hidemi

doi:10.1111/j.1440-1819.1975.tb02318.x

Cited by 6 publications

(5 citation statements)

References 9 publications

(1 reference statement)

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“…The adjunctive use of a DCI with levodopa is another cause of a steep increase in the plasma levodopa concentration when compared to use of levodopa alone [40]. A higher incidence of central nervous system side effects was reported in patients on levodopa/DCI therapy when compared with those on levodopa alone [28,30].…”

Section: Problems Occurring In Advanced Pdmentioning

confidence: 99%

Initial therapy for Parkinson's disease: levodopa vs. dopamine receptor agonists

Kondo

2002

Journal of Neurology

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Levodopa therapy is essential for patients in the advanced stages of Parkinson's disease. However, at early stages, DA agonist therapy has similar efficacy in the treatment of parkinsonism and a lower incidence of motor complications compared to levodopa therapy several years after the initiation of the therapy. The main factors causing motor complications have been speculated to be a severe reduction of dopaminergic nerve terminals because of disease progression, and a pulsatile stimulation of DA receptors using a drug with a short plasma half-life. DA agonists have longer plasma half-lifes than levodopa; therefore, they are expected to have a favorable effect on motor complications. Moreover, two clinical reports confirmed the potential neuroprotection by DA agonists. Although the patient's conditions should be considered in the selsction of a drug, DA agonist therapy is recommended as the initial therapy for Parkinson's disease.

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Section: Problems Occurring In Advanced Pdmentioning

confidence: 99%

Initial therapy for Parkinson's disease: levodopa vs. dopamine receptor agonists

Kondo

2002

Journal of Neurology

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“…apomorphine but not to i.v. apomorphine; (2) prevention of peripheral conversion of l -DOPA to DA by the peripheral decarboxylase inhibitor carbidopa concomitantly reduces blood DA concentration and emesis despite increasing brain DA levels, although vomiting is often not completely prevented in either patients, dogs or least shrews; (3) the peripherally acting D 2 antagonist domperidone in doses up to 40 μg/kg can only partially reduce apomorphine-induced vomiting in beagle dogs, whereas the CNS permeable D 2 antagonist risperidone at 10 μg/kg completely prevented the vomiting; and (4) peripheral injection of direct-acting and selective D 2/3 agonists causes emesis and induces Fos expression in the NTS and DMNX but not in the AP region of the least shrew (Ray, Chebolu, and Darmani, submitted for publication). This finding suggests that DA probably causes vomiting by acting on D 2/3 receptors located on neurons whose dendrites extend from the NTS into the AP.…”

Section: Dopamine: Synthesis Storage Release Degradation and Receptorsmentioning

confidence: 99%

Evidence for a Re-Evaluation of the Neurochemical and Anatomical Bases of Chemotherapy-Induced Vomiting

2009

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“…WT and OCA1 mice were supplemented with a solution containing l -DOPA (Sigma Aldrich, UK) and carbidopa (Sigma Aldrich, UK), dissolved in ddH2O drinking water with ascorbate (2.5 mg/ml) to prevent oxidation, for 28 days starting on PND15 (Table 1 ). l -DOPA is co-administered with carbidopa in order to minimize systemic side effects that can be experienced from l -DOPA exposure alone 34 . The doses selected were based on current l -DOPA use in amblyopia 28 and were calculated as HED following the protocol described by Nair and Jacob 35 .…”

Section: Methodsmentioning

confidence: 99%

Human equivalent doses of l-DOPA rescues retinal morphology and visual function in a murine model of albinism

Sanchez-Bretano,

Keeling,

Scott

et al. 2023

Sci Rep

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Abstractl-DOPA is deficient in the developing albino eye, resulting in abnormalities of retinal development and visual impairment. Ongoing retinal development after birth has also been demonstrated in the developing albino eye offering a potential therapeutic window in humans. To study whether human equivalent doses of l-DOPA/Carbidopa administered during the crucial postnatal period of neuroplasticity can rescue visual function, OCA C57BL/6 J-c2J OCA1 mice were treated with a 28-day course of oral l-DOPA/Carbidopa at 3 different doses from 15 to 43 days postnatal age (PNA) and for 3 different lengths of treatment, to identify optimum dosage and treatment length. Visual electrophysiology, acuity, and retinal morphology were measured at 4, 5, 6, 12 and 16 weeks PNA and compared to untreated C57BL/6 J (WT) and OCA1 mice. Quantification of PEDF, βIII-tubulin and syntaxin-3 expression was also performed. Our data showed impaired retinal morphology, decreased retinal function and lower visual acuity in untreated OCA1 mice compared to WT mice. These changes were diminished or eliminated when treated with higher doses of l-DOPA/Carbidopa. Our results demonstrate that oral l-DOPA/Carbidopa supplementation at human equivalent doses during the postnatal critical period of retinal neuroplasticity can rescue visual retinal morphology and retinal function, via PEDF upregulation and modulation of retinal synaptogenesis, providing a further step towards developing an effective treatment for albinism patients.

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L-Dopa Therapy Combined with Peripheral Decarboxylase Inhibitor (MK-486) in Parkinsonism

Cited by 6 publications

References 9 publications

Initial therapy for Parkinson's disease: levodopa vs. dopamine receptor agonists

Initial therapy for Parkinson's disease: levodopa vs. dopamine receptor agonists

Evidence for a Re-Evaluation of the Neurochemical and Anatomical Bases of Chemotherapy-Induced Vomiting

Human equivalent doses of l-DOPA rescues retinal morphology and visual function in a murine model of albinism

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