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)

Fourteen slightly disabled patients with Parkinsonism were treated separately with benzhexol, amantadine, and levodopa. Benzhexol and amantadine both gave a 15% reduction in functional disability and levodopa a 36% reduction. Benzhexol lessened the rigidity and improved the flexion of posture of Parkinson's disease, but had little or no effect on akinesia and tremor. Amantadine and levodopa caused improvement in all these symptoms. The combination of benzhexol and amantadine was as effective after four weeks of treatment as levodopa was after six months.
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PMID:Comparative trial of benzhexol, amantadine, and levodopa in the treatment of Parkinson's disease. 483 13

A double-blind cross-over study was carried out in 54 patients with Parkinson's disease to evaluate the efficacy of amantadine hydrochloride as compared to a lactose placebo in the management of this illness. Amantadine proved to be a useful and safe addition to the armamentarium when given in daily doses of 200 mg. Forty-eight per cent of patients experienced moderate to good results while 31% showed no measurable improvement. The quality of the improvement was inferior to that obtained with levodopa, but the side effects were fewer. The study could not demonstrate a useful synergistic action between the two drugs, nor could the response to amantadine be used to predict that with levodopa. On the other hand, the addition of amantadine was useful in a few instances where optimal therapeutic doses of levodopa could not be given because of side effects. The mechanism of action of amantadine is still conjectural, but there is strong evidence to indicate some interaction with central dopamine metabolism.
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PMID:Amantadine-HCl (Symmetrel) in the management of Parkinson's disease: a double-blind cross-over study. 493 44

Parkinson's disease is an illness occurring in the third stage of life. At times, the patient suffers from arteriosclerosis as well. Reconstruction processes caused by aging are under way in the brain, which affect, among others, the synapses and transmitter substances. The biotransformation of medication may be changed in elderly persons. The tendency to multimorbidity leads to consumption of several drugs at the same time, possibly causing interference symptoms. Changes in transmitter balance and receptor excitability are, however, the main causes of the toxic side-effects of anti Parkinson therapy. The greater the nigrostriatal degeneration, the lower the tolerance level. Recently, in addition to basic therapy consisting of reduced doses of combined dopa preparations and/or Amantadine sulphate, dopaminergic agonists are used, which act on the receptors which have been maintained. This prevents some side-effects and stabilizes the patient's unpleasant daily fluctuations. Reducing the dosage prevents dyskinesia. pharmacotoxic psychoses require neuroleptics of the Thiaxanthen group or change-over to i.v. Amantadine sulphate infusions or Lisuride i.v.
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PMID:[Toxic drug effects of antiparkinson therapy and their preventability]. 652 82

The effects of anticholinergic and dopaminergic drugs used for Parkinson's disease were studied on the tremor induced by physostigmine (0.3-3.0 mg/kg) in rats. For the measurement of tremor a new electronic device was employed. Atropine (0.3-1.2 mg/kg) and biperiden (0.01-1.0 mg/kg) reduced the physostigmine-induced tremor in a dose-related manner and could abolish it. Biperiden was less potent than atropine. Methylatropine in a dose of 1.2 mg/kg slightly inhibited the tremor. Amantadine (0.3-3.0 mg/kg) reduced the tremor but only to a certain degree. Bromocriptine (0.1-10.0 mg/kg) reduced it in a manner that was not dose-related. Pimozide potentiated the tremor in the dose of 0.2 mg/kg but not in larger doses. At the onset of the tremor, a small decrease in rectal temperature occurred. The hypothermia lasted significantly longer than the tremor. Neither the anticholinergic nor the dopaminergic anti-Parkinson drugs altered the hypothermic effect of physostigmine. The results show that those anti-Parkinson drugs, which act by increasing the dopaminergic activity can counteract the tremor induced by physostigmine. However, these drugs are clearly less active than th anticholinergic anti-Parkinson drugs.
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PMID:Drugs for Parkinson's disease reduce tremor induced by physostigmine. 662 15

Amantadine is useful for the prevention and treatment of influenza A and for the treatment of Parkinson's disease and drug-induced extrapyramidal disorders. We have compared the pharmacokinetics of amantadine in patients with impaired or negligible renal function to that in normal subjects. The half-life of elimination in subjects with normal renal function was 11.8 +/- 2.1 hours (range, 9.7 to 14.5 h). Eight patients with various degrees of renal insufficiency (creatinine clearance from 43.1 to 5.9 mL/min . 1.73 m2) had half-lives of elimination from 18.5 h to 33.8 days. We also studied 10 patients on thrice-weekly hemodialysis. Assuming complete bioavailability of the drug, less than 5% of the dose was removed by each 4-hour hemodialysis. The mean half-life of elimination during chronic hemodialysis was 8.3 days (range, 7.0 to 10.3). We present guidelines for use of amantadine in patients with impaired renal function, including those on maintenance hemodialysis.
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PMID:Pharmacokinetics of amantadine hydrochloride in subjects with normal and impaired renal function. 721 1

Patients with Parkinson's disease were treated with different antiparkinsonian drugs and the amino acid levels in serum and cerebrospinal fluid were determined. Results obtained in 43 patients (L-dopa [26]; prodipine [6]; amantadine [11]) are reported. All drugs investigated produced an increase in amino acids in serum and in CSF, this enhancement being most pronounced for neutral, long-chain amino acids. Amantadine, however, showed this effect for a short period, only. Our results lead us to assume that this increased pool of amino acids in the CSF facilities the biosynthesis of amines with transmitter function from their precursor amino acids.
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PMID:[Comparison between the effects of L-dopa, prodipine and amantadine on the serum and CSF amino acid levels in Parkinson's disease (author's transl)]. 722 2

Amantadine was introduced for the pharmacological management of neuroleptic malignant syndrome (NMS) because of its beneficial effects in Parkinson's disease which were attributed to dopaminomimetic properties. While the dopaminomimetic effects of amantadine are weak under experimental conditions, recent studies have confirmed that amantadine is an antagonist at the N-methyl-D-aspartate (NMDA) type of the glutamate receptor. Amantadine has psychotomimetic properties in patients with Parkinson's disease and normal controls. Two of four patients who received amantadine for NMS suffered an exacerbation of their psychiatric illness. Our observations support the glutamate hypothesis of schizophrenia which suggests that reduced glutamatergic transmission causes a relative dopaminergic excess in the basal ganglia and the limbic system.
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PMID:Amantadine and the glutamate hypothesis of schizophrenia. Experiences in the treatment of neuroleptic malignant syndrome. 810 Oct 93

Amantadine (1-amino-adamantane) is clinically used for the management of Parkinson's disease and drug-induced extrapyramidal symptoms. It has previously been shown that amantadine is a low-affinity uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist with rapid blocking and unblocking channel kinetics (Ki-value at the PCP binding site = 10 microM). The aim of the present studies was to estimate concentrations of amantadine in the central nervous system under therapeutic conditions. In homogenates of postmortem human brain tissue the amantadine concentration appeared to be homogeneously distributed over a wide range of brain areas. Amantadine concentration increased with duration of treatment and decreased wit drug-free time. When the duration of treatment was > or = 10 days and drug-free time < or = 3 days, mean amantadine concentrations in postmortem brain tissue ranged from 48.2 to 386 microM. In contrast to brain tissue, amantadine concentration in cerebrospinal fluid (CSF) and serum was in the low micromolar range ( < 17 microM). CSF and serum total values were highly correlated to each other and were always lower in CSF. The mean CSF/serum ratio for total amantadine was 0.76. To further estimate the extracellular concentration, amantadine was determined in microdialysates in the rat striatum. At behaviorally active doses, amantadine concentration in striatal microdialysates ranged between 6 and 21 microM. These results indicate that extracellular concentrations of amantadine (CSF and serum values in patients, striatal microdialysates in the rat) are in the range of its Ki-value at the PCP binding site. Amantadine concentrations in brain tissue are much higher, probably due to intralysosomal accumulation.
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PMID:Therapeutic brain concentration of the NMDA receptor antagonist amantadine. 853 38

Amantadine has been used for more than 20 years in the symptomatic treatment of Parkinson's disease (PD). Several recent discoveries suggest that amantadine could also have a neuroprotective effect in PD. We studied survival in all parkinsonism (including PD and other parkinsonian syndromes) patients attending a single clinic, employing standard survival curves and a Cox regression model, to identify independent predictive variables for survival (while taking into account factors potentially associated with both outcome and treatment selection). Amantadine-treated patients (n = 250) were similar to the patients not treated with amantadine (n = 586) in terms of age, gender, type of parkinsonism, Hoehn and Yahr stage and dementia status at initial neurological visit. Amantadine use was an independent predictor of improved survival (p < 0.01). Improved survival was also associated with a higher 10-year expected survival (based on age, gender, and birth year), absence of dementia, type of parkinsonism = PD, and low Hoehn and Yahr stage (I or II) at initial neurologic visit (all p < 0.01); these additional factors occurred in statistically similar proportions in the groups that were and were not treated with amantadine. The association of improved survival with amantadine use may stem from symptomatic benefit or may reflect a "neuroprotective" effect, mediated through N-methyl-D-aspartate (NMDA) receptor antagonism, dopamine uptake blockade activity, or other mechanisms. Our preliminary findings suggest that a prospective, controlled, randomized trial of amantadine's effects on PD progression is warranted.
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PMID:Amantadine treatment is an independent predictor of improved survival in Parkinson's disease. 864 47

The effect of amantadine (an antiparkinsonian agent) on calmodulin-dependent cyclic nucleotide phosphodiesterase isozymes was investigated. Amantadine inhibited bovine brain 60 kDa calmodulin-dependent cyclic nucleotide phosphodiesterase but not the bovine brain 63 kDa, heart and lung calmodulin-dependent cyclic nucleotide phosphodiesterase isozymes. The inhibition of bovine brain 60 kDa calmodulin-dependent cyclic nucleotide phosphodiesterase was overcome by increasing the concentration of calmodulin. This suggests that amantadine may be an antagonist of calmodulin or act specifically and reversibly on the action of calmodulin. The bovine brain 60 kDa calmodulin-dependent cyclic nucleotide phosphodiesterase isozyme is predominantly expressed in the brain and its inhibition may result in increased intracellular levels of cyclic AMP (cAMP). The increased intracellular levels of cAMP have a protective role for dopaminergic neurons. The present findings suggest that amantadine may be a valuable tool to investigate the physiological role of 60 kDa calmodulin-dependent cyclic nucleotide phosphodiesterase isozyme in the progression of Parkinson's disease and gives a new insight into the action of this drug.
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PMID:Amantadine: an antiparkinsonian agent inhibits bovine brain 60 kDa calmodulin-dependent cyclic nucleotide phosphodiesterase isozyme. 913 29


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