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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 55 (1990), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Ferritin levels were measured in postmortem brain tissue from patients dying with Parkinson's disease [treated with L-3,4-dihydroxyphenylalanine (L-DOPA)] and from control patients. Ferritin levels were decreased in the substantia nigra, caudate-putamen, globus pallidus, cerebral cortex, and cerebellum when compared with age-matched control tissues. However, in CSF from L-DOPA-treated patients and in serum from L-DOPA-treated and untreated parkinsonian patients, ferritin levels were normal. Previous studies have suggested an increased total iron content in substantia nigra of parkinsonian brain. The failure of substantia nigra ferritin formation to be stimulated by increased iron levels suggests some defect in iron handling in this critical brain region in Parkinson's disease. The reason for decreased ferritin levels throughout the parkinsonian brain is not clear but does not seem to reflect a general system deficit in ferritin.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Oxidative damage has been implicated in the pathology of Parkinson's disease (PD), e.g., rises in the level of the DNA damage product, 8-hydroxy-2′-deoxyguanosine, have been reported. However, many other products result from oxidative DNA damage, and the pattern of products can be diagnostic of the oxidizing species. Gas chromatography/mass spectrometry was used to examine products of oxidation and deamination of all four DNA bases in control and PD brains. Products were detected in all brain regions examined, both normal and PD. Analysis showed that levels of 8-hydroxyguanine (8-OHG) tended to be elevated and levels of 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FAPy guanine) tended to be decreased in PD. The most striking difference was a rise in 8-OHG in PD substantia nigra (p = 0.0002); rises in other base oxidation/deamination products were not evident, showing that elevation in 8-OHG is unlikely to be due to peroxynitrite (ONOO−) or hydroxyl radicals (OH•), or to be a prooxidant effect of treatment with l-Dopa. However, some or all of the rise in 8-OHG could be due to a change in 8-OHG/FAPy guanine ratios rather than to an increase in total oxidative guanine damage.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 113 (1991), S. 8698-8704 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 43 (1978), S. 153-160 
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Plasma growth hormone (GH) concentrations in Parkinsonian patients following 3 months optimum therapy with bromocriptine showed no significant change from pretreatment values, whilst plasma prolactin concentrations were uniformly suppressed. Pretreatment GH and prolactin levels were unrelated to clinical disability, and no correlation between hormonal changes and therapeutic response was found. These results suggest the presence of different dopaminergic receptor mechanisms for GH and prolactin release as well as between the extrapyramidal and neuroendocrine systems.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 54 (1982), S. 105-110 
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Although (−)-deprenyl is known to be metabolized to methamphetamine and amphetamine, two small-scale double-blind trials indicate that neither metabolite contributes to the therapeutic benefit conferred by this drug in certain patients with Parkinson's disease: the manipulation of urinary pH, which alters the rate of excretion of these metabolites, failed to change the response pattern; substitution of a metabolite mixture for active drug caused a falling off in benefit.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neural transmission 43 (1978), S. 245-251 
    ISSN: 1435-1463
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Serial tyramine challenges were given to 4 patients with Parkinson's disease who had taken 10 mg of a selective monoamine oxidase B inhibitor, (-)deprenyl, for up to eighteen months. In doses sufficient for complete inhibition of the platelet enzyme, no clinically significant adverse pressor reactions (“cheese effects”) occurred nor were any significant tyramine responses seen when higher doses of deprenyl (40–60 mg daily) were given for three weeks. A balanced crossover study in six healthy young male adults showed that (-)deprenyl was associated with a significant increase in the frequency of periods of wakefulness and stage 2 sleep and a significant decrease in REM sleep and sleep stages 3 and 4. In 85 patients with Parkinson's disease taking 10 mg of (−) deprenyl daily with levodopa and carbidopa for up to eighteen months, a mean dosage reduction of 200 mg levodopa daily was possible; 19 of the 39 patients who had end-of-dose akinesia responded favourably and only one of the 10 patients with on-off oscillations improved. On 10 mg (-)deprenyl daily only 4 patients showed an “amphetamine response”, but this was more frequent when 40 mg deprenyl was given daily. In 5 patients taking 40 mg (-)deprenyl daily without other medications a mild antiparkinsonian response occurred comparable to that seen with amphetamine.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-2072
    Keywords: Monoamine oxidase inhibitor ; Monoamine oxidase ; ‘Cheese effect’ ; Depression ; Parkinson's disease ; Levodopa ; Phenylethylamine ; Dopamine ; Deprenyl
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract After pretreatment with the selective monoamine oxidase B inhibitor, (-)-deprenyl, in doses sufficient for complete inhibition of the platelet enzyme, 4 normal and 6 parkinsonian volunteers (2 receiving levodopa and 2 levodopa plus carbidopa) suffered no adverse pressor reaction (‘cheese effect’) after challenge with oral tyramine in amounts considerably greater than those likely to be encountered in a normal diet. Nor did the levodopa-deprenyl combination itself result in a pressor response. Normal human intestinal mucosa was shown predominantly to contain the deprenyl-insensitive A form of the enzyme, which presumably degraded administered tyramine in the deprenyl-treated volunteers; even those receiving the drug for prolonged periods manifested no ‘cheese effect’, suggesting that the A form remained uninhibited. Intestinal monoamine oxidase A was able to oxidise dopamine, whereas in human platelet or striatum the amine is a monoamine oxidase B substrate. Like tyramine, oral phenylethylamine challenge with amounts greater than those known to be present in a normal diet similarly gave rise to no adverse reaction in (-)-deprenyl-treated subjects; the reasons for this remain to be determined.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0533
    Keywords: Post-encephalitic parkinsonian syndrome (PEPS) ; Idiopathic Parkinson's disease (PD) ; Substantia nigra ; Age ; I-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In 12 cases of post-encephalitic parkinsonian syndrome (PEPS) starting at a mean age of 25.1 years, the mean disease duration of 35.8 years was twice as long as in 12 young patients with Lewy body-Parkinson's disease (LB-PD), whose disease started at a mean age of 39.9 years (mean duration 16.5 years). In PEPS the rate of progression of disease was extremely slow. The groups were of a similar age at death, but the post-encephalitic cases had 70% fewer cells in the substantia nigra than in idiopathic Parkinson's disease (PD) and 92% fewer than in controls. Nigra cell destruction was not found in PEPS, but active cell breakdown and abundant extraneuronal melanin were present in PD. A second group of 12 LB-PD cases with mean onset at 58.9 years survived for a mean of 10.1 years, but the number of remaining substantia nigra cells was the same as in the young onset cases of PD. This clinical and pathological evidence does not support the notion that progression of disease in PD can be attributed to the superadded effects of normal ageing on top of a primary acute noxious insult sustained in earlier life.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 243 (1996), S. 667-670 
    ISSN: 1432-1459
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Journal of neurology 245 (1998), S. S1 
    ISSN: 1432-1459
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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