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The most frequently used drugs are levodopa, biperiden and selegiline. The total cost reached values of 116,346,589.30 euros during the study period. The CID was 4,14 euros. It was very high the daily treatment cost of pramipexol and entacapone. The prevalence of Parkinson's disease is considered in 1.7 per 1,000 inhabitants in Spain. There is an important geographical variability; regions as Castilla-Leon, Galicia and La Rioja have a higher prevalence than Andalucia or Murcia. The number of patients in Spain can be considered in 69,571 people.
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To test the impact of deprenyl on ischemia-induced changes in vitro, we followed the time course of propidium iodide (PI) uptake as an indicator of neuronal cell death as well as the expression of apoptotic factors in organotypic hippocampal slice cultures exposed to oxygen-glucose deprivation (OGD) for 45 min.
Although basic research has revealed many mechanisms involved in the repair or elimination of damaged neurons, turning these mechanisms into clinically useful neuroprotective interventions is a slow process. Numerous neurotrophic factors seem to mediate neuronal repair and viability, but because the neurotrophic factors are proteins or polypeptides, they cannot be given orally and do not enter the brain if given intravenously. Tapping into the neuroprotective potential of the neurotrophic factor mechanisms must await further developments. Similarly, pharmacological agents that protect damaged neurons by reducing glutamate excitotoxicity, by scavenging free radicals, or by increasing adenosine inhibitory influences, are not ready yet for widespread clinical use. Also, appropriate therapeutic protocols for currently available neuroprotective agents such as vitamin E, selegiline, and NSAIDs remain to be determined. Given the rate of advance of research in this area, however, meaningful neuroprotection and neurorescue will be attainable in the very near future. In the meantime, neuron damaging oxidative stress can be kept in check by insuring adequate dietary sources of antioxidants. Although there is as yet little or no scientific evidence that dietary antioxidants are neuroprotective, the consumption of high antioxidant foods, such as blueberries and strawberries, is appealing to most people regardless of any neuroprotective potential.
Greater improvement was observed after 6 weeks in patients treated with transdermal selegiline than in those given placebo according to all measures. A statistically significant difference between drug and placebo was seen in Hamilton depression scale and Montgomery-Asberg Depression Rating Scale scores as early as week 1 of treatment. There were no differences in the adverse event profile of the patients given selegiline and those given placebo with the exception of application-site reactions, which were more common with the selegiline transdermal system. No orthostatic hypotensive or hypertensive reactions were observed.
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In patients with moderately severe impairment from Alzheimer's disease, treatment with selegiline or alpha-tocopherol slows the progression of disease.
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The goal of this study was to examine the multiple-dose pharmacokinetics of selegiline and its metabolites desmethylselegiline, 1-methamphetamine, and 1-amphetamine after oral administration of selegiline HCl. Twelve healthy volunteers received 10 mg of selegiline HCl once daily for 8 days. The pharmacokinetic profiles of selegiline and the metabolites were examined from serum samples for 24 hours (i.e., the dosing interval, tau) on days 1, 4, and 8. The results indicated significant apparent accumulation of selegiline and desmethylselegiline during the 8-day period of selegiline administration. The AUC tau S of selegiline and desmethylselegiline were increased 2.7 fold (p < 0.001) and 1.5 fold (p < 0.001), respectively, from day 1 to day 8. However, the half-lives of selegiline (range, 1.5-3.5 h) and desmethylselegiline (range, 3.4-5.3 h) were found to be relatively short. Accordingly, the short half-lives of these compounds failed to predict the apparent accumulation. With both of the 1-amphetamine metabolites of selegiline, steady state was reached by day 4. We suggest that the most likely explanation for the apparent accumulation of selegiline and desmethylselegiline was the saturation of the MAO-B binding sites in tissues, although decreased first-pass metabolism of selegiline cannot be ruled out. The observed increase in selegiline and desmethylselegiline concentrations on multiple dosing is not likely to significantly increase the pharmacodynamic effect or adverse effects of selegiline compared with what has been found after a single 10-mg dose.
Agents that are currently available in Canada to treat the cognitive deficits of AD include donepezil, ginkgo biloba, selegiline, and ergoloid mesylates. Donepezil and ginkgo biloba are associated with a statistically significant but clinically modest improvement in cognitive function in a substantial minority of patients with mild to moderate AD. Selegiline may have a mild beneficial effect on cognitive function in some patients with AD, but the data are inconclusive. Ergoloid mesylates have questionable efficacy in AD and can only be recommended as a last line of treatment. The results of a single trial suggest that vitamin E or selegiline (both have antioxidant properties) may slow the progression of AD. Antipsychotic medications can result in clinically significant improvement in agitation and psychosis. Carbamazepine also appears to be an effective treatment for agitation in AD, and there is preliminary evidence that the selective serotonin reuptake inhibitor citalopram reduces irritability in this disorder. There is no evidence that other nonneuroleptic medications are more efficacious than placebo in treating agitation in AD. Limited data indicate that depression in dementia responds to antidepressant medication.
In order to investigate the conversion of selegiline (SG), a drug used in the treatment of Parkinson's disease, to selegiline N-oxide (SGO) as a major metabolic pathway for SG, rat liver microsomal incubations were carried out in vitro in the presence of NADPH. SG was transformed into SGO in vitro as described in our previous human in vivo experiment. In the kinetic studies, the Vmax/Km value of the N-oxidation at pH 8 was found to be approximately four times greater than that at pH 7.4. The N-oxidation was also found to be inhibited by methimazole, an inhibitor of the flavin-containing monooxigenase (FMO) rather than by SKF 525A, an inhibitor of cytochrome P450s, and stimulated approximately two times by n-octylamine, an stimulator of FMO. Moreover, the N-oxidation activity remained almost unchanged in the presence of NADPH even after heating at 50 degrees C for a few minutes. The present data demonstrate that the N-oxidation of SG to SGO is principally mediated by FMO.
This study found a differential compliance and persistence across PD drug therapies. The compliance rate for rasagiline was significantly higher than that for all of the other PD medications. In addition, rasagiline and levodopa/carbidopa/entacapone were associated with significantly higher persistence rates than were the other PD medications.