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Eldepryl (Selegiline Hydrochloride)
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Eldepryl

Eldepryl is a medication which inhibits the breakdown of a chemical in your brain called dopamine, and thereby prevents Parkinson's disease.

Other names for this medication:

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Also known as:  Selegiline Hydrochloride.

Description

Eldepryl is a medication which prevents the breakdown of a chemical in your brain.

Eldepryl is used to treat Parkinson's disease.

Eldepryl is also known as Selegiline.

Eldepryl prevents the breakdown of a chemical in your brain called dopamine, thereby prevents Parkinson's disease.

Brand names of Eldepryl are Eldepryl, Zelapar.

Dosage

Take Eldepryl orally.

Take Eldepryl capsules twice a day, at breakfast and lunch.

Do not swallow the tablet whole. Allow it to dissolve in your mouth without chewing.

Do not drink or eat anything for at least 5 minutes after takink Eldepryl.

While using Eldepryl, you must not eat foods that are high in tyramine such as air dried meats, aged or fermented meats, sausage or salami (including cacciatore and mortadella), pickled herring, and any spoiled or improperly stored beef, poultry, fish, or liver; beer from a tap, beer that has not been pasteurized; aged cheeses, including blue, boursault, brick, brie, camembert, cheddar, emmenthaler, gruyere, parmesan, romano, roquefort, stilton, and swiss; sauerkraut, soy beans, soy sauce, tofu, miso soup, bean curd, fava beans; yeast extracts (such as Marmite).

Preferable food during Eldepryl usage are fresh meat, poultry, or fish (including lunch meat, hot dogs, breakfast sausage, and cooked sliced ham); any vegetables except broad bean pods (fava beans); processed cheese, mozzarella, ricotta, cottage cheese; pizza made with cheeses low in tyramine; soy milk, yogurt.

If you want to achieve most effective results do not stop taking Eldepryl suddenly.

Overdose

If you overdose Eldepryl and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Eldepryl overdosage: severe headache, hallucinations, vision problems, sweating, cool or clammy skin, fast or uneven heart rate, feeling light-headed, fainting, seizure.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Eldepryl are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Eldepryl if you are allergic to Eldepryl components.

Do not take Eldepryl if you are pregnant, planning to become pregnant or breast-feeding.

Be careful using Eldepryl if you have kidney disease, liver disease, heart disease, high or low blood pressure, seizure disorder.

Be careful using Eldepryl if you take over-the-counter medications you use, including vitamins, minerals, and herbal products, carbamazepine (Tegretol), diet pills or cold medicines that contain ephedrine, pseudoephedrine or phenylephrine, nafcillin (Unipen), phenobarbital (Luminal, Solfoton), rifampin (Rifadin, Rifater, Rifamate, Rimactane), antidepressants such as amitriptyline (Elavil), amoxapine (Ascendin), bupropion (Wellbutrin, Zyban), citalopram (Celexa), clomipramine (Anafranil), desipramine (Norpramin), doxepin (Sinequan), duloxetine (Cymbalta), escitalopram (Lexapro), fluoxetine (Prozac), fluvoxamine (Luvox), imipramine (Tofranil), nortriptyline (Pamelor), paroxetine (Paxil), protriptyline (Vivactil), sertraline (Zoloft), venlafaxine (Effexor) or trimipramine (Surmontil).

While using Eldepryl, you must not eat foods that are high in tyraminesuch as air dried meats, aged or fermented meats, sausage or salami (including cacciatore and mortadella), pickled herring, and any spoiled or improperly stored beef, poultry, fish, or liver; beer from a tap, beer that has not been pasteurized; aged cheeses, including blue, boursault, brick, brie, camembert, cheddar, emmenthaler, gruyere, parmesan, romano, roquefort, stilton, and swiss; sauerkraut, soy beans, soy sauce, tofu, miso soup, bean curd, fava beans; yeast extracts (such as Marmite).

Do not take Eldepryl if you use over-the-counter supplements or cough and cold medicines that contain tyramine.

It can be dangerous to stop Eldepryl taking suddenly.

eldepryl drug classification

Two (11)C-labelled PET tracers, (R)-N-[(11)C]methyl-N-(3,3-dideuteropropargyl)-1-phenylpropan-2-amine ([(11)C]L-deprenyl-D2, [(11)C]DED) and (S)-N-[(11)C]methyl-N-propargyl-1-phenylpropan-2-amine ([(11)C]D-deprenyl, [(11)C]DDE) were synthesised. One step N-alkylation with [(11)C]MeI or [(11)C]MeOTf was performed using the automated platform TRACERlab® FX-C Pro. The labelled products were obtained with (37±15)% (n=10) (end of synthesis, decay corrected from [(11)C]MeI) radiochemical yields from [(11)C]MeI after 38±3min synthesis time. In all cases, radiochemical purity was over 99% when [(11)C]MeOTf was used. This synthesis using a commercial platform makes these tracers more accessible for clinical research purposes.

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This was a randomized controlled study in which patients enrolled within two weeks of stroke underwent a clinical and functional evaluation and a neuropsychological assessment. The patients were given selegiline (10mg/day) or matched placebo once a day for six weeks in addition to standard rehabilitation care.

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(-)Deprenyl has been proposed to be neuroprotective to dopamine neurons in the parkinsonian brains. To clarify the mechanism, the effects of (-)deprenyl and structurally related compounds on apoptosis induced by a neurotoxin, N-methyl(R)-salsolinol, and reactive oxygen species, nitric oxide and peroxynitrite, were examined in dopaminergic SH-SY5Y cells. DNA damage was quantified by the single cell gel electrophoresis (comet) assay. (-)-Deprenyl protected the cells from apoptosis in a dose-dependent way, which required pre-treatment at least for 20 min. The effect was confirmed even after washing out of (-)deprenyl, indicating that (-)-deprenyl initiates the intracellular process to antagonize the apoptotic death program. The studies on the structure-activity relationship reveal that N-propargyl residue with hydrophobic structure is essential for the anti-apoptotic function. These results suggest that (-)deprenyl and related compounds may be applicable as neuroprotective agents in neurodegenerative diseases.

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We performed a double-blind parallel study of deprenyl 5 mg BID vs. placebo in treatment of "on-off" oscillations complicating Parkinson's disease. After a 2-week baseline period, treatment was given for 6 weeks with weekly evaluations using the Northwestern Disability Scale and patients' hourly self-assessment of "on-off" status performed at home. Patients on deprenyl experienced significant improvement in time spent in the "on" state. They were also more likely than patients on placebo to experience improvement of severity of tremor and hypomimia during the "on" state. No other areas of disability improved in quality. Side effects such as hallucinations and worsening of choreoathetosis were frequent among the deprenyl group but generally responded to reduction in concomitant levodopa/carbidopa dosage. We conclude that deprenyl is moderately useful in ameliorating "on-off" in a majority of patients.

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STN DBS at γ frequencies (MED and MOVE) and HF significantly improved mUPDRS scores compared to no stimulation and both γ frequencies were not different from HF. DBS at θ and β frequencies did not worsen mUPDRS scores compared to no stimulation.

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Time-activity data from lung and arterial plasma were used from seven nonsmokers and seven smokers scanned previously with CLG and D CLG, and five nonsmokers and nine smokers scanned previously with DEP and D DEP. The measured time-activity curves for lung and plasma and the integrals for the arterial plasma time-activity curves were compared at an early time point (2.5 min) and at the end of the study (55 min). A three-compartment irreversible model was used to estimate the differences between smokers and nonsmokers, and the stability of the parameter (k(3)) while varying model assumptions for the relative fractions of lung tissue, blood and air in the PET voxel.

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Cardiovascular baroreceptor responsiveness of conscious rats treated with selective inhibitors of monoamine oxidase (MAO) types A and B was determined by measurement of blood pressure (BP) and heart rate (HR) responses to intravenous injection of phenylephrine and sodium nitroprusside. Treatment with selegiline (1 or 5 mg/kg p.o. daily for 7 days) did not significantly modify resting levels of BP and HR, lower or upper HR plateau levels, or HR/BP gain. Treatment with clorgyline (2 mg/kg p.o. daily for 7 days) increased HR/BP gain but also did not modify resting BP or HR, or lower and upper plateau levels of HR. The results are compatible with an effect of MAO-A inhibition to modify monoamine levels in medullary areas participating in CNS control of blood pressure.

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The effects of acute catechol-O-methyltransferase (COMT) inhibition on L-DOPA pharmacokinetics were studied in 10 parkinsonian subjects on stable doses of L-DOPA/carbidopa and selegiline. Tolcapone, a reversible COMT inhibitor, was administered in four single ascending doses (50-800 mg) randomly paired with placebo. Serial plasma concentrations of L-DOPA and its metabolites were measured, and patient diaries and clinical ratings of dyskinesia were completed every 30 min for 6 h. Tolcapone increased the area under the curve of the plasma L-DOPA concentration versus time curve and decreased the accumulation of homovanillic acid. COMT inhibition increased "on" time and the duration of dyskinesia without affecting the maximal amplitude of dyskinesia. Tolcapone may be a useful adjunct to L-DOPA/carbidopa.

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Levodopa is still the most effective therapeutic agent for the treatment of Parkinson's disease (PD). Initially, levodopa provides a stable therapeutic response but, during long-term treatment its beneficial effect declines and a gradually increasing number of patients experience fluctuations in motor response. Therefore, in the management of PD it is important to minimise the risks for the development of motor fluctuations. In this context, recent double-blind long-term studies have confirmed the earlier results, suggesting that it appears advisable to initiate dopaminergic treatment in early PD by initially using a dopamine agonist and by adding levodopa when the benefit is no longer adequate with dopamine agonist alone. Another alternative would be to start with selegiline alone, then depending on the disability of the patient, add a dopamine agonist and finally levodopa.

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A sensitive and specific assay for the quantitative determination of amphetamine, methamphetamine and desmethyldeprenyl in human plasma specimens is described. Electron capture/negative ion chemical ionization gas chromatography/mass spectrometry is used to determine the extracted plasma concentrations of the three target compounds as their N-heptafluorobutyryl derivatives. Quantitation is performed by stable isotope dilution using d6-amphetamine and d6-methamphetamine as internal standards. Selected ion monitoring of the [M-HF]- ions of both the analytes and internal standards results in minimum quantifiable limits of 0.10 ng ml-1 for both amphetamine and methamphetamine and 0.25 ng ml-1 for desmethyldeprenyl. Excellent linearity (r = 0.998) up to at least 5.00 ng ml-1 is demonstrated.

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Monoamine oxidase (MAO) A and B are important enzymes that metabolize biogenic amines throughout the body. Previous studies had suggested that both MAO A and B consist of two subunits of molecular masses of 63 and 60 kilodaltons, respectively. The cDNAs encoding one subunit of human liver MAO A and B have been expressed in mammalian cells by transfection of the individual clones. The proteins expressed from these cDNAs are shown to be catalytically active. Similar to the endogenous enzymes, the expressed MAO A prefers serotonin as a substrate and is sensitive to the inhibitor clorgyline. In contrast, the expressed MAO B prefers phenylethylamine as a substrate and is sensitive to the inhibitor deprenyl. These results suggest that a single polypeptide of MAO A (or B), existing as either a monomer or homodimer, is enzymatically active. The ability to obtain functional MAO A and B from their respective cDNA clones allows us to study further the structure and function relationships of these important enzymes.

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Articles retrieved were reviewed and selected for inclusion based on their being randomized, double-blind, placebo-controlled studies that appeared between the years 2000 and 2007 and examined efficacy, safety, and tolerability data from clinical trials of patients with MDD who were treated with the STS. Four articles, including 3 acute trials and 1 long-term prevention of relapse trial, were included in this review based on these criteria.

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Monoamine neurotransmitter systems, along with cholinergic systems, are known to play important roles in cognition, and are disrupted in at least some patients with dementia of the Alzheimer type (DAT). This suggests that monoamine-enhancing drugs might ameliorate cognitive symptoms in certain patients with DAT. L-Deprenyl is a monoamine oxidase (MAO) inhibitor which may selectively inhibit MAO-B at low doses, while at high doses it nonselectively inhibits MAO-A as well as MAO-B. We studied its effects on several types of cognitive function in 17 patients with DAT. Two doses of L-deprenyl (10 mg/day and 40 mg/day) and placebo were compared in a double-blind, serial treatment design. Episodic learning and memory, knowledge memory, attention, recognition, and performance on a continuous performance task were assessed at baseline and under these drug and placebo conditions. Statistically significant improvement was noted in performance on an episodic memory and learning task requiring complex information processing and sustained conscious effort during treatment with L-deprenyl 10 mg/day. Knowledge memory, intrusions, and other cognitive functions relevant to DAT were not altered by L-deprenyl at either dose.

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Patients meeting DSM-IV criteria for MDD (N = 265) were randomly assigned to blinded treatment with STS or a matching placebo patch for 8 weeks. Patients failing to meet or maintain protocol-defined therapeutic response criteria at predetermined time points had their STS (or placebo) dose increased. Assessments were conducted at weeks 1, 2, 3, 5, 6, and 8. Patients were not required to follow a tyramine-restricted diet. The study ran from September 2001 through August 2002.

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The ejaculatory response and other components of the 5-hydroxytryptamine (5-HT) behavioural syndrome induced by 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) (3 mg kg-1, i.p.) were studied following single and repeated treatment of rats with eight different monoamine oxidase (MAO) inhibitors. Single and repeated treatment with the 5-HT agonist 5-MeODMT, and with low doses of the potent releaser of 5-HT, p-chloroamphetamine (PCA) were also included in the study. Repeated but not single treatment with 5-MeODMT reduced strongly but reversibly the ejaculatory response and the behavioural responses. Repeated but not single treatment with the nonselective and irreversible MAO inhibitors nialamide and pargyline reduced markedly the ejaculatory response but only slightly the 5-HT behavioural responses. Repeated treatment with the irreversible MAO-B inhibitor (-)-deprenyl, with the irreversible MAO-A inhibitor, clorgyline, with the reversible MAO-A inhibitor moclobemide, and with low doses of PCA did not affect either of the responses. Repeated but not single combined treatment with clorgyline plus PCA caused an almost complete blockade of all the four responses. The selective and reversible MAO-A inhibitors (as well as 5-HT releasers) amiflamine, alpha-ethyltryptamine, and alpha-methyltryptamine reduced markedly the ejaculatory response after both single and repeated treatments. The behavioural responses were blocked only after repeated treatment. It is concluded that single and repeated treatments of rats with different MAO inhibitors do not produce a common alteration in 5-HT2 receptor functions. Repeated treatment with 5-MeODMT caused a blockade of 75-95% of the ejaculatory response and 5-HT behavioural responses. A similar strong blockade was only produced by the combined effect of MAO-A inhibition and 5-HT release.

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The objectives of this study were to assess potential pharmacokinetic and pharmacodynamic interactions between moclobemide and selegiline. Two groups of 12 healthy male and female subjects were treated with 200 mg moclobemide or 5 mg selegiline b.i.d. for 16 days. On study day 8, the alternative active drug or placebo was added to the respective treatments. Concentration-time profiles of moclobemide and two of its main metabolites and 3,4-dihydrox/phenylglycol (DHPG, a norepinephrine metabolite), 5-hydroxy-indoleacetic acid (HIAA, a serotonin metabolite), and 3,4-dihydroxyphenylacetic acid (DOPAC, a dopamine metabolite) in plasma as well as MAO-B activity and serotonin concentration in platelets were determined at steady state during monotreatment and combined treatment. The pharmacokinetic parameters of moclobemide and its metabolites changed on multiple dosing but were not influenced to a relevant extent by concomitant administration of selegiline. The measured pharmacodynamic parameters, expressed as the maximum effect on a study day and the area under the effect-time curve, characterized the drugs' influence on peripheral neurotransmitter metabolism. The most reliable variables to assess inhibition of MAO-A and -B in humans proved to be DHPG in plasma and serotonin in platelets and MAO-B activity in platelets, respectively. Several variables (DHPG, platelet serotonin) suggested that selegiline has some MAO-A inhibitory activity. This became particularly apparent upon addition of selegiline to moclobemide treatment; i.e., the effects of combined moclobemide and selegiline treatment were statistically greater than those of moclobemide monotreatment. Moclobemide alone exerted a slight inhibition of platelet MAO-B activity. The reported pharmacodynamic interactions are not considered to be clinically relevant. However, due to the previously found supraadditive tyramine potentiation upon simultaneous treatment, moclobemide and selegiline should only be combined when applying dietary restrictions with respect to tyramine.

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Because of the number of different types of anti-Parkinsonian medications, a number of options in the treatment of PD are now available. Each patient's medication regimen should be individualized. Many of the medication choices are made based on the stage of the disease. For patients who have newly diagnosed PD, and who are on no medications, treatment with deprenyl should be strongly considered. While some controversy remains concerning its possible slowing of the rate of disease progression, there is no evidence to suggest that its use is detrimental. It is generally well tolerated in patients with early disease. These factors must be weighed against the cost of the medication, and the fact that little if any therapeutic effect is seen in most patients who are not being treated with LD. A useful analogy when considering this issue is the prophylactic use of aspirin for cerebrovascular or cardiovascular disease. Newly diagnosed patients requiring treatment, who have tremor as their only symptom or their most prominent symptom, may be given an anticholinergic medication. Patients who have significant bradykinesia, rigidity or gait disturbance can be given amantadine. A combination of these two medications may be useful, and a combination of deprenyl with an anticholinergic drug or amantadine may provide excellent relief of early symptoms. At some point, most patients' symptoms progress such that treatment with LD is considered. Given its possible, but unproven, acceleration of the rate of disease progression, this decision should be weighed carefully. In a relatively young patient who may be treated for many years, a dopamine receptor agonist can be initiated without LD therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

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Parkinson's disease involves the progressive degeneration of dopamine neurons in the extrapyramidal motor system. Levodopa, the metabolic precursor of dopamine, relieves symptoms but does not prevent continued cell death. Research suggests that monoamine oxidase B inhibitors, such as selegiline, should benefit Parkinson's patients. Evidence to date indicates that selegiline improves the effectiveness of levodopa and may even slow cell death.

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A prospective, randomized, placebo-controlled, double-blind, parallel-group, 6-month study assessed the efficacy and safety of ropinirole, a nonergoline D2-dopamine agonist, in patients with early Parkinson's disease (n = 241; Hoehn & Yahr stages I to III) with limited or no prior dopaminergic therapy. Patients (mean age, 62.8 years), stratified by concomitant use of selegiline, were randomized to ropinirole (n = 116) or placebo (n = 125). The starting dose of ropinirole was 0.25 mg tid with titration to at least 1.5 mg tid (maximum dose, 8 mg tid). Primary efficacy endpoint was the percentage improvement in Unified Parkinson's Disease Rating Scale (UPDRS) motor score. Ropinirole-treated patients had a significantly greater percentage improvement in UPDRS motor score than patients who received placebo (+24% vs -3%; p < 0.001). Ropinirole was well tolerated and patient withdrawals were infrequent. Most adverse experiences were related to peripheral dopaminergic activity. Ropinirole monotherapy is an effective and well-tolerated therapeutic option for treatment of early Parkinson's disease.

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Blood pressure and heart rate responses to oral tyramine have been measured in healthy volunteers before and after administration of the selective monoamine oxidase B inhibitor selegiline at high dosage (30 mg/day). Treatment brought about a 2 to 4-fold increase in tyramine sensitivity and a concomitant small but significant reduction in plasma 4-hydroxy-3-methoxyphenylglycol concentration, pointing to the emergence of some degree of monoamine oxidase A inhibition. It is suggested that patients treated with selegiline 30 mg/day or more should be placed on a tyramine-free diet.

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The results suggest that isatin and (-)-deprenyl have some common target genes and this supports the idea that isatin may be an endogenous partial functional agonist of (-)-deprenyl. Since GAPDH mRNA expression is sensitive to the pharmacological treatments, these results also question the applicability of GAPDH as a reference gene in gene expression studies.

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Monoamine oxidases play a central role in catecholamine catabolism in the central nervous system. The biochemical and pharmacological properties of inhibitors of the monoamine oxidase type B are reviewed. The evidence for biochemical activities distinct from their ability to inhibit MAO-B is discussed, including possible antioxidative and antiapoptotic activities of these agents. The significance of these properties for the pharmacological management of Parkinson's disease and the evidence for a neuroprotective effect of one such agent (selegiline) is also discussed.

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The role of plasma homovanillic acid together with serum growth hormone and prolactin in monitoring of central dopaminergic activity was studied in healthy volunteers and psychiatric patients. Both dopaminergic agonists (apomorphine, bromocriptine and L-dopa) and antagonists (metoclopramide) were used. Apomorphine, bromocriptine and metoclopramide, which exerted the expected neuroendocrine effects caused no significant changes in plasma homovanillic acid. L-dopa increased the concentration of homovanillic acid in plasma. This effect was not potentiated by L-deprenyl, although L-dopa-induced growth hormone secretion was increased after L-deprenyl premedication. There was negative correlation between growth hormone secretion and the increase of plasma homovanillic acid after L-dopa. This indicates that the L-dopa-induced rise in plasma homovanillic acid probably reflects more peripheral L-dopa metabolism than central dopaminergic activity. Thus, it seems that plasma homovanillic acid cannot be regarded as a sensitive indicator of drug-induced changes in central dopaminergic activity in man, which is in contrast with some earlier findings in animals.

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Despite the large amount of neuropharmacological data concerning catecholamine (CA) mechanisms of the mammalian brain, little is known yet about the effects of MAO-inhibitors on single neurons. The present series of experiments aim to elucidate these specific neurochemical attributes of forebrain cells. Single neuron activity was recorded by means of multi-barreled microelectrodes in the caudate nucleus, globus pallidus, and amygdala of both anesthetized rats and anesthetized or alert monkeys during microelectrophoretic application of the MAO-B blocker L-deprenyl (DEPR). CAs (dopamine and noradrenaline), glutamate, GABA, and acetylcholine were also applied. Nearly the half (46%) of all forebrain neurons tested responded, exclusively with inhibition, to DEPR, and the CA-sensitive cells were especially responsive to the MAO-B inhibitor. The time course of DEPR-induced neuronal suppression was short. In some cases, amphetamine (AMPH) and clorgyline (CLOR) were also applied microelectrophoretically. AMPH elicited similar activity changes to those seen after DEPR administrations, whereas CLOR applications were less effective. Our results provide evidence that DEPR can effectively modulate the activity of CA-sensitive neurons in the three different forebrain regions of two different species. On the basis of this data, the possible neurochemical mechanisms of DEPR action are discussed.

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The effects of lesions of the substantia nigra (electrolytic 2 mA 10 sec, or 6-OHDA 2 or 8 micrograms) and of the midbrain raphé nuclei (electrolytic 2 X 1.0 mA 10 sec) at 7 days postlesion on striatal levels of beta-phenylethylamine, DA, DOPAC, HVA, 5-HT and 5-HIAA and on hypothalamic levels of beta-phenylethylamine, DA, NA, 5-HT and 5-HIAA were investigated. In the presence of deprenyl (2 mg kg-1 2 hr SC), both electrolytic and 6-OHDA-induced dopamine-depleting lesions of the nigra but not 5-HT-depleting lesions of the raphé nuclei resulted in a marked decrease in the accumulation of beta-phenylethylamine. The marked reduction in accumulation of striatal beta-phenylethylamine in response to lesions of the substantia nigra indicates that the intraneuronal compartment is a major site of striatal beta-phenylethylamine synthesis. An equivalent decrease (approximately 40%) in the accumulation of 5-HT was observed following electrolytic lesions of the substantia nigra or raphé nuclei after administration of L-5-HTP (200 mg kg-1 hr IP). As L-5-HTP at the dose employed in this study is taken up non-selectively by both DA- and 5-HT-containing neurones the loss of L-AAD following nigral and raphé lesions was apparently equivalent. These results indicate that depletion of beta-phenylethylamine may not be simply attributable to a general loss of L-AAD following lesions of monoamine-containing neurones and suggest either co-localisation of beta-phenylethylamine and DA or the existence of distinct beta-phenylethylamine-containing neurones.

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Depletion of noradrenaline in locus coeruleus neurons after reserpinization was prevented by clorgyline, a selective inhibitor of MAO A, but not by deprenyl, a selective inhibitor of MAO B. Only MAO A is therefore responsible for the degradation of homoneuronal noradrenaline in locus coeruleus nerve cells.

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eldepryl drug 2016-01-20

A recent study by the Parkinson's Disease Research Group of the United Kingdom revealed higher mortality in patients with Parkinson's disease who were treated with selegiline (deprenyl) compared with those who were not. In this article, the methodological limitations of the UK study are discussed. Although several problems exist with this study, the mortality rate was correct, since the data were obtained from a verifiable source. The question then is whether or not the higher mortality rate can be ascribed to selegiline. It is difficult to find answers to this question in the study data, and we will have to wait for the study authors' final report. No other studies have reported higher mortality with selegiline. However, when prescribing selegiline in patients with early-stage Parkinson's disease, it is important to provide them with all the available information so that treatment decisions can be made jointly. Meanwhile, the buy eldepryl online best indication for selegiline appears to be motor fluctuations in patients with moderately advanced Parkinson's disease.

eldepryl and alcohol 2016-10-28

We determined whether food restriction or the drugs nimodipine (Ca2+ antagonist) and deprenyl (a MAO-B inhibitor) prevent the development of stroke in the spontaneously hypertensive stroke-prone rat (SHR-SP). Forty male SHR-SP rats, in the age of 34 weeks, were exposed to various treatments. During a period of 27 weeks, survival and blood pressure were followed. In the control and deprenyl group, the blood pressure values remained unchanged; 50% had died after 27 weeks. All rats that were treated with nimodipine survived. After food restriction, 7/8 rats survived and showed a lower blood pressure. This study in SHR-PR rats shows the superiority of nimodipine on survival, and the buy eldepryl online potential of food restriction as a stroke-preventing measure.

eldepryl drug interactions 2017-01-28

Monoamine oxidase (MAO) inhibitors were the first antidepressants introduced, but their use has dwindled because of their reported side effects, buy eldepryl online their food and drug interactions, and the introduction of other classes of agents. However, interest in MAO inhibitors is reviving. Here, we discuss their use, risks, and benefits in clinical medicine.

eldepryl dosage 2016-06-19

We examined the relationship between buy eldepryl online severity of depression in Parkinson's disease (PD) and regional cerebral blood flow (rCBF) using single photon emission computed tomography (SPECT) and the reaction to levodopa-selegiline combination therapy.

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(-)-Deprenyl (0.25 or 2 mg/kg) or saline was injected daily into male Wistar rats for 3 weeks. The striata were dissected out and soluble and particulate superoxide dismutase activity measured. (-)-Deprenyl at 2 mg/kg induced a significant increase in the soluble but not the particulate form buy eldepryl online of the enzyme. The possibility that this action contributes to the ability of (-)-deprenyl to retard nigral degeneration in man and prolong life in rats is discussed.

eldepryl generic name 2015-08-13

The observations showed that in the course of human buy eldepryl online kidney transplantation necrotic, apoptotic and proliferating renal tubular cells can be observed. All calcium channel blockers and (-)-deprenyl decreased the occurrence and degree of apoptosis in rat kidney.

eldepryl dosage forms 2016-12-12

Parkinson's disease (PD) is a progressive neurodegenerative, dopamine deficiency disorder. The main therapeutic strategies for PD treatment relies on dopamine precursors (levodopa), inhibition of dopamine metabolism (monoamine oxidase [MAO] B and catechol-O-methyl transferase inhibitors), and dopamine receptor agonists. Recently, a novel selective and irreversible MAO B propargylamine inhibitor rasagiline (N-propargyl-1-R-aminoindan, Azilect((R))) was approved for PD therapy. In contrast to selegiline, the prototype of MAO B inhibitors, rasagiline is not metabolized to potentially toxic amphetamine metabolites. The oral bioavailability of rasagiline is 35%, it reaches T(max) after 0.5-1 hours and its half-life is 1.5-3.5 hours. Rasagiline undergoes extensive hepatic metabolism primarily by cytochrome P450 type 1A2 (CYP1A2). Rasagiline is initiated at 1 mg once-daily dosage as monotherapy in early PD patients and at 0.5-1 mg once-daily as adjunctive to levodopa in advanced PD patients. Rasagiline treatment was not associated with "cheese effect" and up to 20 mg per day was well tolerated. In PD patients with hepatic impairment, rasagiline dosage should be carefully adjusted. Rasagiline should not be administered with other MAO inhibitors and co-administration with certain antidepressants and opioids should be avoided. Although further clinical evidence buy eldepryl online is needed on the neuroprotective effects of rasagiline in PD patients, this drug provides an additional tool for PD therapy.

eldepryl cost 2015-11-15

Previously, we have reported that L-deprenyl decreased the incidence of mammary tumors and pituitary tumors in old acyclic rats. The objective of the present study was to investigate the effects of L-deprenyl, a monoamine oxidase-B (MAO-B) inhibitor, treatment on the development and growth of tumors and on the metabolism of catecholamines and indoleamine in the medial basal hypothalamus (MBH) and the striatum (ST) of rats bearing 7,12-dimethylbenzanthracene (DMBA)-induced mammary tumors. Female Sprague-Dawley rats with DMBA-induced mammary tumors were injected (sc) daily with 0.25 mg or 5.0 mg of deprenyl/kg BW or the vehicle (saline; control) for 12 wk. Tumor diameter, tumor number, body weight, and feed intake were measured every week of the treatment period. Serum PRL and the concentrations of catecholamines, indoleamine, and their metabolites were measured by RIA and HPLC, respectively. Treatment with 5.0 mg deprenyl decreased the tumor diameter, tumor number, and serum prolactin (PRL) level. Although the body weight increased in all three groups, the body weight gain in the 5.0 mg group was smaller than that in the control and 0.25 mg groups. Deprenyl treatment had no effect on feed intake. The concentrations of dihydroxyphenylacetic buy eldepryl online acid (DOPAC) and homovanillic acid (HVA) were decreased in the MBH and the ST, and the concentration of 5-hydroxyindoleacetic acid (5-HIAA) was decreased in the MBH of deprenyl-treated rats. Treatment with 5.0 mg deprenyl enhanced the concentrations of norepinephrine (NE) and serotonin (5-HT) in the MBH and in the ST, and the concentration of dopamine (DA) in the MBH. These results suggest that the suppression of the development and growth of DMBA-induced mammary tumors by chronic deprenyl treatment may be mediated through alterations in the synthesis and metabolism of catecholamines and indoleamine in the MBH and inhibition of PRL secretion.

eldepryl syrup 2016-01-28

The acetylenic selective monoamine oxidase (MAO) type B suicide inhibitor, l-deprenyl (l-selegiline), has proved to be a useful adjuvant to L-dopa therapy and monotherapy of Parkinson's disease. Although not all features of its antiParkinson action are known, studies that used brains obtained at autopsy from patients who took l-deprenyl show that the selective inhibition of MAO-B with a concomitant increase of phenylethylamine and dopamine, but not of serotonin or noradrenaline, in the basal ganglia may be responsible for its mode of action. The increased life expectancy noted in patients with Parkinson's disease who received long-term therapy (9 years in an uncontrolled study) is another unexpected feature of the drug. These exciting data, if confirmed in other long-term clinical trials, may herald a neuroprotective approach to the treatment of this degenerative disease. More recent studies indicate that Parkinson's disease may eventually turn out to be a neurotoxic event resulting from oxidative stress-induced free radical species in the substantia nigra. Thus selective MAO-B inhibitors could represent a unique class of drugs, having symptomatic actions with buy eldepryl online possible neuroprotective and neurorescue actions in one.

eldepryl order 2017-02-01

This paper reviews the toxicokinetics of amphetamines. The designer drugs MDA (methylenedioxy-amphetamine, R,S-1-(3;,4;-methylenedioxyphenyl)2-propanamine), MDMA (R,S-methylenedioxymethamphetamine), and MDE (R,S-methylenedioxyethylamphetamine), as well as BDB (benzodioxolylbutanamine; R,S-1-(1;,3;-benzodioxol-5;-yl)-2-butanamine or R,S-1-(3;,4;-methylenedioxyphenyl)-2-butanamine) and MBDB (R,S-N-methyl-benzodioxolylbutanamine), were taken into consideration, as were the following N-alkylated amphetamine derivatives: amphetaminil, benzphetamine, clobenzorex, dimethylamphetamine, ethylamphetamine, famprofazone, fencamine, fenethylline, fenproporex, furfenorex, mefenorex, mesocarb, methamphetamine, prenylamine, and buy eldepryl online selegiline. English-language publications from 1995 to 2000 were reviewed. Papers describing identification of metabolites or cytochrome P450 isoenzyme-dependent metabolism and papers containing pharmacokinetic/toxicokinetic data were considered and summarized. The implications of toxicokinetics for toxicologic assessment or for interpretation in forensic cases are discussed.

eldepryl dosing 2016-07-23

In a previous communication the results of a three months clinical trial with the co-administration of the Beta-type Monoamineoxydase (MAO)-inhibitor L-deprenyl in long-term levodopa treated Parkinsonian patients were reported. In view of the favourable effects observed in this study, as well as in others, L-deprenyl was continued in this patient group and given to other patients, found suitable, for periods of four years and more. In the 29 patients reported here, special attention buy eldepryl online was addressed to fluctuating manifestations of chronic levodopa therapy. Apart from a considerable subjective improvement, L-deprenyl effected an objective improvement in the overall disability score as well as an appreciable reduction of "on-off" phenomena in the great majority of the patients. Dyskinesias appeared in 4 of the patients and increased mildly in another ten. Untoward effects of L-deprenyl were not serious, mostly transitory, and none was prohibitive. In 13 of the 29 patients (44.83%) the levodopa dose could be reduced by 26.5% +/- 0.46, while in two patients it was raised from 250 mgm to 462.5 mgm daily. The present and previous clinical studies show that L-deprenyl is a valuable adjunctive agent for the long-term levodopa treated parkinsonian patient.

cost of eldepryl 2015-10-10

Full generalization to the methamphetamine-training stimulus was produced by an i.m. dose of 10.0 mg/kg p-fluoro-L-deprenyl. L-Deprenyl and the metabolites of p-fluoro-L-deprenyl, p-fluoro-L-amphetamine, and p-fluoro-L-methylamphetamine were more potent, producing full generalization at doses of 1.0-3.2 mg/kg. Under the FR10 schedule of drug injection, persistent self-administration behavior was maintained by i.v. cocaine injections but not by injections of vehicle or injection doses of p-fluoro-L-deprenyl up to 1.0 mg/kg. However, p-fluoro-L-deprenyl did maintain moderate levels of i.v. self-administration responding under the second-order schedule of drug injection. Peak response rates maintained by 0.1-mg/kg injections of p-fluoro-L-deprenyl were significantly greater than those associated with saline substitution, yet significantly lower than those maintained buy eldepryl online by cocaine or D-amphetamine.

eldepryl medication dose 2015-06-11

Sexually inactive ("low-performing," LP) and highly active ("high-performing," HP) rats were selected from a sexually inexperienced population. Saline control LP rats (n = 44) lived 134.58 +/- 2.29 weeks, their HP peers (n = 49) lived 151.24 +/- 1.36 weeks. Life-long treatment with 0.25 mg/kg (-)deprenyl, a selective inhibitor of MAO-B that also stimulates action potential- buy eldepryl online transmitter release coupling in the catecholaminergic neurons in the brain (catecholaminergic activity enhancer, CAE, effect), enhanced the sexual and learning performance of both LP and HP rats and prolonged their life. LP rats (n = 48) treated with (-)deprenyl lived 152.54 +/- 1.36 weeks and HP rats on (-)deprenyl (n = 50) lived 185.30 +/- 1.96 weeks. As an indicator of the basic activity of catecholaminergic neurons, the resting release of dopamine from the striatum, substantia nigra, and tuberculum olfactorium, and of norepinephrine from the locus coeruleus, was measured in 2-, 4-, 8-, 16-, and 32-week-old male and female rats. The release of transmitters between weaning and the second month of age, i.e., during the crucial developmental phase of life, was significantly higher than either before or after that period, indicating that a CAE mechanism starts working with high intensity after weaning, lasts until the completion of full scale sexual development, and shows an unparalleled decay thereafter. It was concluded that the CAE regulation in the brain, stimulated by (-)deprenyl, controls general activity and consequently the longevity of rats.

eldepryl tablets 2017-02-02

Twenty parkinsonian patients were selected for a short-term, single-blind, cross-over trial. Each patient received one of the two brands of selegiline, Parkryl (Mei-Shih), 10 mg per day as an adjunct to Madopar. After a 6-week treatment period and a 4-week wash-out buy eldepryl online period, the treatment was switched to the other brand of selegiline, Jumexal (Labatec), for another 6 weeks.

eldepryl medication 2017-08-09

To analyze the dispensation of antiparkinsonian agents in Spain and to Periactin Pills Online estimate the Parkinson's disease prevalence.

eldepryl drug classification 2015-11-06

Mean (+/- SD) cabergoline was increased from 6.43 +/- 2.66 to 12.78 +/- 5.67 mg/day and mean L-dopa reduced from 606.6 +/- 263.9 to 370.6 +/- 192.5 mg/day. A significant reduction (P < 0.001) in mean hyperkinesia intensity occurred from baseline (day 0) to week 26. Improvements in 'on with dyskinesias', mean dystonia intensity (P < Zantac 500 Mg 0.05), time spent in 'severe off' condition, severity of 'off' periods as well as clinical/patient global impression, and health-related quality of life were observed. Twenty-four drug-related adverse events were recorded of which four were regarded as serious.

eldepryl buy 2016-01-13

We have examined mitochondrial membranes and molecular hallmarks of apoptosis in response to increasing concentrations of 1-Methyl, 4-phenyl, Pyridinium ion (MPP(+)) in SK-N-SH neurons and have evaluated the neuroprotective potential of Selegiline Cardura Prostate Medication with a primary objective to explore its mechanism(s) of neuroprotection. MPP(+)-induced apoptosis was characterized by spherical appearance, suppressed neuritogenesis, phosphatidyl serine externalization, plasma membrane perforations, mitochondrial membrane potential (Delta Psi) collapse, mitochondrial aggregation, and nuclear DNA fragmentation and condensation. At lower concentrations, MPP(+) (10-100 microM) produced mitochondrial swelling and loss of cristae, and at higher concentrations (300-500 microM), degeneration and aggregation of mitochondrial membranes in the peri-nuclear region, which were attenuated by Selegiline (10-50 microM) pre-treatment. At still higher concentrations, MPP(+) (>500 microM) produced necrotic changes represented by mitochondrial and plasma membrane ballooning and perforations. Selegiline provided partial neuroprotection at higher concentrations of MPP(+). MPP(+)-induced increases in reactive oxygen species, lipid peroxidation, cytochrome-C release, necrosis factor kappa-B (NF-kappa-B) activation, 8-hydroxy, 2 deoxy guanosine synthesis, alpha-synuclein indices, and reductions in glutathione, ATP, and superoxide dismutase were attenuated by Selegiline. Selegiline also attenuated MPP(+)-induced transcriptional activation of c-fos, c-jun, GAPDH, and caspase-3, suggesting that it may provide neuroprotection by preserving mitochondrial membranes, by attenuating molecular markers of apoptosis, by scavenging free radicals, and by regulating immediate early genes involved in neurodegeneration.

eldepryl generic 2016-08-13

N-Methyl,N-propargyphenylethylamine (MPPE) is a novel analog of (-)-deprenyl, a drug prescribed for Parkinson's disease and shown to have neuroprotective and neurorescue properties in a wide variety of in vitro and in vivo models. MPPE is also neuroprotective, but has the advantage over (-)-deprenyl of not being metabolized to amphetamine Glucophage 1000mg Tab or N-methylamphetamine.

eldepryl 5 mg 2015-09-20

An endogenous dopamine-derived N-methyl(R)salsolinol has been suggested to be involved in the pathogenesis of Parkinson's disease. In Parkinson's disease, the level of N-methyl(R)salsolinol increased in cerebrospinal fluid and the high activity of a synthesizing enzyme, (R)salsolinol N-methyltransferase, was detected in lymphocytes. This isoquinoline induced apoptotic DNA damage in human dopaminergic neuroblastoma SH-SY5Y cells. Among catechol isoquinolines, only N-methylsalsolinol induced apoptosis in the cells, and the scavengers of hydroxyl radicals and antioxidants suppressed DNA damage, suggesting that reactive oxygen species initiate apoptosis. The isoquinoline activated caspase-3 like proteases and a caspase-3 inhibitor protected the cells from DNA damage. (-)Deprenyl, but neither clorgyline nor Prograf 1mg Cost pargyline, prevented apoptotic cell death. The mechanism of the protection was due to stabilization of mitochondrial membrane potential reduced by the toxin. In Parkinson's disease apoptosis may be induced in dopamine neurons by this endogenous neurotoxin, and (-)deprenyl may protect them from apoptotic death process.

eldepryl reviews 2016-03-15

First line antidepressants are the so-called SSRIs (selective serotonin reuptake inhibitors), e.g. fluvoxamine, fluoxetine, sertraline, paroxetine and escitalopram. Unfortunately, these drugs mostly do not provide full symptom relief and have a slow onset of action. Therefore other antidepressants are also being prescribed that inhibit the reuptake of norepinephrine (e.g. reboxetine, desipramine) or the reuptake of both serotonin (5-HT) and norepinephrine (e.g. venlafaxine, duloxetine, milnacipran). Nevertheless, many patients encounter residual symptoms such as Imodium Generic impaired pleasure, impaired motivation, and lack of energy. It is hypothesized that an impaired brain reward system may underlie these residual symptoms. In agreement, there is some evidence that reuptake inhibitors of both norepinephrine and dopamine (e.g. methylphenidate, bupropion, nomifensine) affect these residual symptoms. In the pipeline are new drugs that block all three monoamine transporters for the reuptake of 5-HT, norepinephrine and dopamine, the so-called triple reuptake inhibitors (TRI). The working mechanisms of the above-mentioned antidepressants are discussed, and it is speculated whether depressed patients with different symptoms, sometimes even opposite ones due to atypical or melancholic features, can be matched with the different drug treatments available. In other words, is personalized medicine for major depression an option in the near future?

eldepryl drug 2015-10-14

Drugs currently approved by the U.S. Food and Drug Administration (FDA) for the treatment of Alzheimer's disease include acetylcholinesterase inhibitor (i.e., tacrine, donepezil, rivastigmine, and galantamine) and glutamate-modulating (i.e., memantine) drugs. Because these drugs have modest benefits, various alternative drug therapies have been of interest. Drugs with vasodilator activity were originally tried in dementia when it was hypothesized that the condition was due to cerebrovascular insufficiency. Isoxsuprine and ergoloid mesylates are FDA approved for the treatment of dementia, although they have limited evidence of benefit and are rarely used. The hypothesis that free radicals may initiate and maintain mechanisms responsible for neurodegeneration in dementia has stimulated interest in investigating various antioxidant and anti-inflammatory drugs. There is no evidence that other drug therapies Diovan 80mg Tablets , including vitamin E, selegiline, nonsteroidal anti-inflammatory drugs, statin drugs, omega-3 fatty acids, estrogen or combined estrogen plus progestin therapy, or B vitamins, are sufficiently effective and safe to justify their clinical use for the treatment of dementing disorders.

eldepryl and alcohol 2017-06-05

Monoamine oxidase (MAO) enzymes catalyze the oxidative deamination of amines and neurotransmitters and inhibitors of MAO are useful as neuroprotectants. This work evaluates the human MAO-catalyzed oxidation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a dopaminergic neurotoxin, to the directly-acting neurotoxic metabolites, 1-methyl-4-phenyl-2,3-dihydropyridinium (MPDP(+)) and 1-methyl-4-phenylpyridinium (MPP(+)) measured by High-Performance Liquid Chromatography (HPLC), and this approach is subsequently used as a new method for screening of MAO inhibitors and protective agents. Oxidation of MPTP by human MAO-B was more efficient than by MAO-A. R-Deprenyl, a known neuroprotectant, norharman (β-carboline), 5-nitroindazole and menadione (vitamin K3) inhibited MAO-B and reduced the formation of toxic pyridinium cations. Clorgyline and the β-carbolines, harman and norharman, inhibited the oxidation of MPTP by MAO-A. Cigarette smoke, as well as the naturally occurring β-carbolines (norharman and harman) isolated from smoke and coffee inhibited the oxidation of Avodart Capsules MPTP by MAO-B and/or MAO-A, suggesting protective effects against MPTP. The results show the suitability of the approach used to search for new MAO inhibitors with eventual neuroprotective activity.

eldepryl drug interactions 2016-10-29

Some authors have suggested that the use of DDD (defined daily doses) of L-dopa may be useful as an indicator of the frequency of Parkinson' Norvasc Online s disease.

eldepryl dosage 2017-09-06

Selegiline, as an adjunct therapy to Madopar, has a moderate effect in prolonging the duration of on-time in parkinsonian patients with Vasaka Tablets dose-related fluctuations. Jumexal seemed to produce no greater effect than Parkryl.