Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A consecutive series of 105 outpatients with Parkinson's disease (PD) were examined for the presence of depression. Twenty-one percent met diagnostic criteria for major depression, 20% had minor depression, and the remainder were not depressed. The frequency of depression showed a bimodal distribution over time, with highest frequencies occurring in the early and late stages of the disease. Although other factors such as a positive family history of psychiatric disorders, quality of social functioning, and severity of tremor, rigidity, and akinesia did not show a significant association with depression, depressed patients had significantly higher impairment scores in activities of daily living and cognitive function than nondepressed PD patients. There was also a significant correlation between impairment and depression scores. In addition, among patients with mainly unilateral symptoms, depression was significantly associated with greater left hemisphere involvement. These findings suggest that depression in the early stages of the disease may be related to left hemisphere dysfunction, while later in the disease, depression and impairment in activities of daily living are interrelated. This may indicate more than one etiology of depression or that depression may have an adverse impact on the course of the disease.
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PMID:Depression in Parkinson's disease. 229 85

Autologous adrenal medulla was transplanted into the putamen of a patient with severe Parkinson's disease. After the operation, the patient's akinesia and rigidity decreased and the duration of action of L-dopa treatment was prolonged. The effect lasted for only 6 months, however, following which the patient's condition gradually began to deteriorate again, returning to the preoperative state by 12 months after surgery. This paper discusses possible reasons why the effect was only temporary.
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PMID:Adrenal medulla transplantation into the putamen in Parkinson's disease. 232 Feb 18

We evaluated neurochemically, behaviorally, and neuropathologically the availability of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated C57 black (BL) mice as a model for Parkinson's disease. The dopamine and 3,4-dihydroxyphenyl acetic acid content in the striatum, measured by high-performance liquid chromatography with an electrochemical detector, decreased by 70% at 10 and 20 days after the withdrawal of MPTP (30 mg/kg, i.p. twice daily for 5 days). During these days, the mice showed a decrease in locomotor activity and exhibited akinesia in both pole and traction tests. Light microscopically, 44% of the MPTP-treated mice showed neuronal degeneration in the substantia nigra 1 month after the withdrawal (damaged group), and 56% showed no change (undamaged group). Morphometric analysis revealed that the number of neurons in the substantia nigra decreased by 33% on the average in both groups. Electron microscopically, an electron-dense degeneration of most neurons was seen in the substantia nigra of the damaged group, and even in the undamaged group, loss of rough endoplasmic reticulum and mitochondrial deformity were seen in 50-70% of the neurons. Electron-dense bodies were seen in the striatum of both groups. These results show the validity of the MPTP-treated C57 BL mice as a suitable model for parkinsonism, including Parkinson's disease.
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PMID:Evaluation of a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated C57 black mouse model for parkinsonism. 235 77

Although it is known that Parkinson's disease results from a loss of dopaminergic neurons in the substantia nigra, the resulting alterations in activity in the basal ganglia responsible for parkinsonian motor deficits are still poorly characterized. Recently, increased activity in the subthalamic nucleus has been implicated in the motor abnormalities. To test this hypothesis, the effects of lesions of the subthalamic nucleus were evaluated in monkeys rendered parkinsonian by treatment with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The lesions reduced all of the major motor disturbances in the contralateral limbs, including akinesia, rigidity, and tremor. This result supports the postulated role of excessive activity in the subthalamic nucleus in Parkinson's disease.
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PMID:Reversal of experimental parkinsonism by lesions of the subthalamic nucleus. 240 38

Treatment of common marmosets with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 1-4 mg/kg for up to 4 days) caused a profound parkinsonian state. Ten days from the start of MPTP treatment, all animals showed marked motor impairment, consisting of bradykinesia and akinesia, limb rigidity, postural abnormalities, loss of vocalisation and blink reflex, and, on occasions, postural tremor. Measurement of caudate-putamen monoamine content at this time showed a profound loss in 3,4-dihydroxyphenylethylamine, homovanillic acid, and 3,4-dihydroxyphenylacetic acid concentrations. Measurement of neuropeptide concentrations in the caudate-putamen, internal and external segments of the globus pallidus, nucleus accumbens, substantia nigra, frontal cortex, and hippocampus showed met-enkephalin, leu-enkephalin, and cholecystokinin (CCK-8) concentrations to be unaffected by MPTP treatment. There was a small decrease in the substance P content of frontal cortex, but otherwise the content of this neuropeptide was unaltered. Parkinsonism in the marmoset, induced by MPTP treatment 10 days earlier, does not alter neuropeptide concentrations in the manner observed in Parkinson's disease.
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PMID:Lack of change in basal ganglia neuropeptide content following subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine treatment of the common marmoset. 242 37

DL-threo-3,4-dihydroxyphenylserine (DL-threo-DOPS) was administered during 10 days to 4 patients with longstanding Parkinson's disease in addition to their treatment with L-3,4-dihydroxyphenyl-L-alanine (L-DOPA)-carbidopa (Sinemet). All patients tended to improve in their symptoms freezing, all day life activity and mood. There were no improvements in rigidity, tremor, and akinesia (in general). During the DL-threo-DOPS-treatment cerebrospinal fluid (CSF), serum and urine concentrations of catecholamines were measured. The results show that DL-threo-DOPS is transported to the brain and CSF in a way comparable with L-DOPA. However, no measurable increase of 3-methoxy-4-hydroxyphenylethyleneglycol (MOPEG) in CSF could be demonstrated. This suggests that the synthesis of noradrenaline from DL-threo-DOPS in the brain is doubtful. In addition measurements in urine reveals that at the dose used Sinemet prevents peripheral decarboxylation of DL-threo-DOPS into noradrenaline. Other possible metabolic pathways of DL-threo-DOPS are discussed.
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PMID:Catecholamine metabolism during additional administration of DL-threo-3,4-dihydroxyphenylserine to patients with Parkinson's disease. 247 57

In order to evaluate in a double-blind manner the therapeutic efficacy of selegiline in the treatment of late-phase Parkinson's disease, 19 patients with end-of-dose type fluctuations were randomized for a double-blind cross-over trial receiving either selegiline 10 mg or placebo. Each period lasted 12 weeks. During a two week prestudy period the dose of levodopa was titrated to optimal levels. The disability was evaluated using the Columbia University Disability Scale (CUDS). The patients kept a daily diary to monitor closely the frequency and severity of their fluctuations and the side-effects of treatment. Their parkinsonian disability and all main symptoms improved significantly during selegiline treatment. The mean duration of action of a levodopa dose was significantly longer and there was significantly less daily end-of-dose and early morning akinesia during selegiline treatment. The side-effects were similar in both treatments. This double-blind study confirms the findings of earlier open studies that selegiline potentiates and prolongs the therapeutic effects of levodopa and thus its use is particularly beneficial in patients with end-of-dose type fluctuations in disability.
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PMID:Selegiline in the treatment of daily fluctuations in disability of parkinsonian patients with long-term levodopa treatment. 251 16

The case of a patient with levodopa-responsive pure akinesia and freezing of gait for 17 years, whose brain showed the classical changes of Lewy body Parkinson's disease at postmortem is presented. A short trial of DL-threo-DOPS was ineffective. Intellectual function was preserved despite the presence of Lewy bodies and mild cell loss in subcortical cholinergic nuclei. Pure akinesia is likely to be a heterogeneous condition, with most cases having little or no response to levodopa therapy. However, this case demonstrates that this clinical picture may be caused by Lewy body Parkinson's disease.
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PMID:Pure akinesia due to lewy body Parkinson's disease: a case with pathology. 229 68

Levodopa (+ dopa decarboxylase inhibitor) is the most active of all drugs used in the treatment of Parkinson's disease. It acts on both akinesia and rigidity and improves the prognosis of the disease by increasing life expectancy. But levodopa also produces late side-effects: it often induces abnormal movements, fluctuations in motor performance, on-off effects, psychotic hallucinations, etc. Since these late side-effects remain difficult to treat, it is always necessary to assess the benefits and risks of the first treatment with levodopa. Anticholinergic drugs, which mainly act on tremor, must be used with caution since they may induce memory alterations and often confusional states in aged parkinsonians. Dopamine agonists are prescribed as adjuvant therapy in the treatment of the late side-effects of levodopa. New drugs (selegiline), new pharmaceutical preparations (sustained release forms), the first treatment of the disease (levodopa alone versus agonists alone versus levodopa + agonists), together with the new pharmacological approaches (brain grafts, drug infusions) are now under clinical evaluation.
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PMID:[Antiparkinsonian drugs]. 256 51

The effect of stimulation of cerebral dopamine D-1 receptors by CY 208-243 on motor disability was tested in MPTP-treated parkinsonian marmosets and patients with Parkinson's disease. CY 208-243 (0.5-1.25 mg/kg s.c.) produced a dose-related reversal of akinesia and rigidity in the marmosets, lasting some 2 h. Single morning doses of CY 208-243 (5-40 mg) were compared with the usual morning dose of levodopa in eight patients with Parkinson's disease on long-term levodopa therapy who had developed motor fluctuations from immobility with akinesia and rigidity (off) to mobility often with dyskinesias (on). CY 208-243 alone was capable of switching such patients from off to on; five of the eight patients responded to the highest dose (40 mg), sometimes with dyskinesias. The response to CY 208-243 was comparable to that produced by levodopa in these cases. Drugs designed to stimulate both dopamine D1 and D2 receptors in the brain may improve the therapy of Parkinson's disease.
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PMID:Antiparkinsonian activity of CY 208-243, a partial D-1 dopamine receptor agonist, in MPTP-treated marmosets and patients with Parkinson's disease. 257 Oct 82


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