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An intermittent, controlled-rate, slow progressive degeneration model of Parkinson's disease: antiparkinson effects of Sinemet and protective effects of methylphenidate.

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The causes of nigrostriatal neuron degeneration in Parkinson's disease (PD) are not known, but it has been suggested that exogenous or endogenous factors or neurotoxins may play a role. The degree of vulnerability to neurotoxins or other potential mediators of nigral dopamine cell death is thought

Excellent response to apomorphine in Parkinsonism with optic atrophy unresponsive to oral antiparkinsonian medication.

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Two patients presented with the cardinal symptoms of Parkinson's disease (PD), which had developed slowly and progressively. One patient underwent brain imaging of the dopaminergic system, the results of which were compatible with PD. However, both patients showed no response to L-dopa or oral

Neuroprotective effect of the antiparkinsonian drug pramipexole against nigrostriatal dopaminergic degeneration in rotenone-treated mice.

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Pramipexole, an agonist for dopamine (DA) D2/D3-receptors, has been used to treat both early and advanced Parkinson's disease (PD). In this study, we examined the effect of pramipexole on DA neurons in a PD model of C57BL/6 mice, which were treated with rotenone (30 mg/kg, p.o.) daily for 28 days.

Antiparkinsonian drugs and dopaminergic neostriatal mechanisms: studies in rats with unilateral 6-hydroxydopamine (=6-OH-DA)-induced degeneration of the nigro-neostriatal DA pathway and quantitative recording of rotational behaviour.

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The symptomatic treatment of multiple system atrophy.

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Multiple system atrophy (MSA) is a neurodegenerative disease of undetermined aetiology that occurs sporadically and manifests itself as a combination of parkinsonian, autonomic, cerebellar and pyramidal signs. Despite the lack of any effective therapy to reverse this condition, some of the symptoms

Management of multiple system atrophy: state of the art.

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Multiple system atrophy (MSA) is a sporadic neurodegenerative disease of undetermined aetiology presenting with parkinsonian, autonomic, cerebellar, and pyramidal signs. Despite the lack of any effective therapy to reverse MSA, some of the symptoms may be improved with adequate symptomatic

Antiparkinson prodrugs.

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Parkinson's disease (PD) is a progressive, neurodegenerative disorder which involves the loss of dopaminergic neurons of the substantia nigra pars compacta. Current therapy is essentially symptomatic, and L-Dopa (LD), the direct precursor of dopamine(DA), is the treatment of choice in more advanced

Striatal monoamine neurotransmitters and metabolites in dominantly inherited olivopontocerebellar atrophy.

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We measured the levels of the monoamine neurotransmitters and metabolites in striatum of 14 patients with end-stage dominantly inherited olivopontocerebellar atrophy (OPCA). On average, dopamine levels were reduced in putamen (-53%), caudate (-35%), and nucleus accumbens (-31%). However, individual

Investigation of Anti Parkinson Activity of Dicyclomine

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Background: Parkinson disease (PD) is progressive neurodegenerative disorder. The major causative factors that progress the PD are age, genetic abnormalities, environmental factors and degeneration of dopamine neurons in substantia nigra. PD normally exerts a tonic inhibitory effect on

Antiparkinsonian drugs and their neuroprotective effects.

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In Parkinson's disease, while dopamine (DA) replacement therapy, such as with L-DOPA (levodopa), improves the symptoms, it does not inhibit the degeneration of DA neurons in the substantia nigra. Numerous studies have suggested that both endogenous and environmental neurotoxins and oxidative stress

Inhibitory effects of antiparkinsonian drugs and caspase inhibitors in a parkinsonian flatworm model.

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It has been known that rotenone and 1-methyl-4-phenylpyridinium ion (MPP(+), a metabolite of MPTP), which inhibit mitochondrial complex I, are useful tools for parkinsonian models in vertebrates such as primates and rodents. Planarian, an invertebrate flatworm, has a high potential for regeneration,

[The effect of a new antiparkinson agent, Selegilin, on psychomotor performance in humans].

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A combination of tests consisting of a compensation task with differential value indication, a tachystoscopic arrangement with verbal identification of characteristic features and an arrangement for a visually induced motor reaction was carried out on 12 healthy volunteers aged from 20-30 to

Cannabinoid CB1 antagonists possess antiparkinsonian efficacy only in rats with very severe nigral lesion in experimental parkinsonism.

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We have observed that systemic administration of cannabinoid CB1 antagonists exerts antiparkinsonian effects in rats with very severe nigral lesion (>95% cell loss), but not in rats with less severe lesion (85-95% cell loss). Local injections into denervated striatum and corresponding globus

Brain dopamine-stimulated adenylyl cyclase activity in Parkinson's disease, multiple system atrophy, and progressive supranuclear palsy.

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The dopamine D(1) receptor is considered to participate in levodopa's antiparkinsonian action and levodopa-induced dyskinesias. We examined the functional status of the D(1) receptor in brain of patients with Parkinson's disease (PD), multiple system atrophy (MSA), and progressive supranuclear palsy

Differential alterations in nicotinic receptor alpha6 and beta3 subunit messenger RNAs in monkey substantia nigra after nigrostriatal degeneration.

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Our previous studies showed that alpha4, alpha6, alpha7, beta2, beta3 and beta4 nicotinic acetylcholine receptor messenger RNAs are present in monkey substantia nigra, with a particularly intense and localized labelling of the alpha6 and beta3 subunit messenger RNAs to this brain region. Because

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