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Eldepryl (Selegiline Hydrochloride)

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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.


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.


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.


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.


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.


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.

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Although the involvement of monoamine oxidase B (MAO-B) in physiological function is not yet well understood, its inhibitors have been shown to be quite useful in the treatment of various neuropsychiatric disorders. Platelet MAO-B activity has been found to be reduced in several psychiatric disorders, related to substance abuse and associated with different personalities. 1-Deprenyl (selegiline), an archetypical MAO-B inhibitor, alone does not seem to exert an antidepressive effect, however, it may become useful when administered in combination with amine neurotransmitter precursors. MAO-B inhibitors are useful adjunct drugs to 1-DOPA in the symptomatic treatment of Parkinson's disease. Interestingly, 1-deprenyl alone can slow down the progress of otherwise disabled syndromes of Parkinson's disease. It has been proposed that 1-deprenyl may play a role in neuroprotection and neurorescue. MAO-B inhibitors can selectively and dramatically increase the level of beta-phenylethylamine, which has been shown to potentiate dopamine and noradrenaline function in the central nervous system. Several new types of highly selective, reversible and irreversible MAO-B inhibitors have recently been developed. The mechanism(s) of neuroprotective and rescue actions of 1-deprenyl and other MAO-B inhibitors will help to shed some light on our understanding of the neurodegenerative process.

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Parkinsonism is an uncommon movement disorder in childhood. Six unusual cases of acquired parkinsonism in hospitalized children are described. Clinical manifestations included an akinetic-rigid syndrome with and without tremor, the combination of parkinsonism and dystonia, and a parkinsonism-plus syndrome. Altered mental status, mutism, dysphagia, and sialorrhea were frequent associations. Etiologies included hypoxic-ischemic encephalopathy; haloperidol treatment with and without neuroleptic malignant syndrome; toxicity of cytosine arabinoside, cyclophosphamide, amphotericin B, and methotrexate; St. Louis encephalitis and other encephalitides; and a pineal tumor with hydrocephalus. Cranial magnetic resonance imaging results ranged from normal to profound cerebral and cerebellar atrophy with chemotherapeutic toxicity. The illnesses usually were severe enough to require pharmacotherapy. Incorrect diagnoses of depression or catatonia delayed treatment or aggravated the problem. Acute treatment included amantadine, levodopa/carbidopa with or without selegiline, diphenhydramine, or benztropine. The concentration of CSF homovanillic acid was normal in a neuroleptic-associated patient, but the level was low in an encephalitic patient. All patients demonstrated dramatic improvement, including two who were not treated; some had complete resolution of symptoms and none required continued antiparkinsonian drugs despite poor scores on the Unified Parkinson's Disease Rating Scale and the Modified Hoehn and Yahr Rating Scales. The causes of parkinsonism described are more common in a general pediatric hospital than the parkinsonism associated with the popularized Segawa syndrome.

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L-deprenyl is a potent, well tolerated and safe inhibitor agent of MAO-B. Administration in daily dosage of 10 mgs produces an almost complete inhibition of the enzyme. Clinical trials of the use of l-deprenyl in Parkinson's disease have shown the following: l-deprenyl as monotherapy in Parkinson's disease does not control its symptoms. In those on a therapeutic regimen containing levodopa and experiencing fluctuating responses, particularly the "wearing off" type, the addition of l-deprenyl results in their attenuation or control. It is not fully agreed by all investigators whether such as effect is enduring or begins to wane after two or three years, nor that other symptoms of parkinsonism are improved. One investigator has reported that the combined use of these agents has resulted in an increase in life expectancy in Parkinson's disease. They have suggested that these findings indicate that l-deprenyl may be capable of preventing degeneration of the nigro-striatal system and halting progression of the Parkinson's disease process. This has raised the issue of initiating treatment with l-deprenyl during the early phases of Parkinson's disease.

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Autonomic nervous system (ANS) involvement is frequently found in Parkinson's disease (PD), but its causal relationship to the disease itself and its medication is unclear. We evaluated the effects of PD medications on cardiovascular ANS functions. Heart rate (HR) responses to normal and deep breathing, the Valsalva manoeuvre and tilting, and blood pressure (BP) responses to tilting and isometric work were measured prospectively in 60 untreated PD patients randomised to receive either levodopa (n = 20), bromocriptine (n = 20) or selegiline (n = 20) as their initial treatment. The results were compared with those of 28 healthy controls. The responses were recorded at baseline, after 6 months on medication and following a 6-week washout period. At baseline HR responses to normal breathing, deep breathing and tilting were already lower and the fall in the systolic BP immediately and at 5 min after tilting was more pronounced in the PD patients than in the controls. Six months' levodopa treatment diminished the systolic BP fall after tilting when compared to baseline, whereas bromocriptine and selegiline increased the fall in systolic BP after tilting and selegiline diminished the BP responses to isometric work. The BP responses returned to the baseline values during the washout period. The drugs induced no change in the HR responses. Thus PD itself causes autonomic dysfunction leading to abnormalities in HR and BP regulation and the PD medications seem to modify ANS responses further. Bromocriptine and selegiline, in contrast to levodopa, increase the orthostatic BP fall and suppress the BP response to isometric exercise reflecting mainly impairment of the sympathetic regulation.

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(-) Deprenyl given in small (0.25 mg/kg) daily doses for 30 days to rats left the serotonin (5-HT) and the 5-hydroxyindoleacetic acid (5-HIAA) levels in the striatum unchanged. The postsynaptic 5-HT receptor responsiveness, as measured with 5-methoxy-N,N-dimethyl-tryptamine (5-MeODMT), remained also unaltered. In (-) deprenyl-treated rats the p-chloroamphetamine (PCA)-induced 5-HT syndrome was significantly increased and this enhancement of the PCA effect was not abolished by the reserpine-induced depletion of the 5-HT stores.

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Patients in selegiline group had less severe disease (UPDRS score 24.11 +/- 14.07) as compared to controls (UPDRS score 40.53 +/- 18.52). There was significant improvement in UPDRS score (p < 0.05), WAIS (p < 0.001) and memory (p < 0.001) in selegiline group. In the control group there was a significant prolongation of P300 latency (p < 0.05).

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Forty-one patients with Parkinson's disease and severe dyskinesias were analyzed retrospectively to determine if some general principles would emerge to aid physicians handling this complication of treatment. Dyskinesia type (high dopa chorea [HDC], low dopa chorea [LDC], high dopa dystonia [HDD], and low dopa dystonia [LDD]) predicted response to treatment and whether or not levodopa dose reduction would benefit dyskinesias without producing unacceptable "offs." High dopa chorea improved best but at the expense of increased "off" time, followed by LDD, HDD, and LDC. Levodopa reduction was an acceptable strategy in ameliorating HDC and LDD only. Adjunctive therapy benefited all dyskinesia types, although the majority of patients (12/17) helped by selegiline had LDD or LDC. Generally, low doses of dopamine agonists were helpful (bromocriptine < 20 mg/day; pergolide < 2 mg/day). When adding adjunctive therapy (except for selegiline or controlled-release carbidopa/levodopa), concomitant reduction in daily dose of levodopa was not an effective strategy to decrease dyskinesias. Serial trials of multiple drug regimens are useful in these patients.

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A new strategy has been developed for synthesizing positron emission tomography (PET) radiotracers using [11C]methyl iodide. This strategy relies on the ability of organic co-solvents to cluster within mixtures of supercritical fluids resulting in localized regions of high density which can serve as microscopic pockets for reaction. We've shown that acetonitrile will cluster about dilute solutes when mixtures of this co-solvent with carbon dioxide are forced to behave as a homogeneous fluid at the critical point. We applied this strategy in a systematic investigation of the conditions for optimized reaction between methyl iodide and L-alpha-methyl-N-2-propynyl phenethylamine (nordeprenyl) to yield L-deprenyl. Variables such as temperature, ultraviolet light exposure, co-solvent concentration, system pressure, and methyl iodide concentration were explored. The synthesis of radioactive [11C]-L-deprenyl using no-carrier-added concentrations of [11C]methyl iodide was also tested. Results showed that greater than 90% radiochemical yield of the desired product could be attained using 40 times less labeling substrate than in conventional PET tracer syntheses.

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Kinetical properties of human placental monoamine oxidase (MAO) were investigated in studies on inhibitors and mixed substrates. MAO activity was determined by a radioisotopic assay. Lineweaver-Burk plots were linear at higher and lower concentrations of PEA, whereas at intermediate substrate concentrations, a downward curving plot was obtained. The Km values of the low- and high-affinity sites for PEA deamination were estimated. Studies with mixed substrates showed that 5-HT was a competitive inhibitor and tyramine a mixed-type inhibitor of deamination at high concentrations of PEA, whereas both were non-competitive inhibitors at lower concentrations of PEA. After pre-incubation of human placental mitochondrial preparations with deprenyl, Lineweaver-Burk plots were completely linear, and the Km value was the same as that obtained at low concentrations of PEA in the absence of deprenyl. Tyramine and 5-HT were competitive inhibitors of PEA deamination by deprenyl-treated MAO. From these results it is concluded that there are two kinds of MAO with high- and low-affinity sites for PEA in mitochondria of human placenta, corresponding to type B and A Mao, and that tyramine, 5-HT and PEA share a substrate-binding site on type A Mao, while tyramine and 5-HT bind to a site on type B MAO that is different from the PEA binding site.

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α-synuclein, a small protein (140 amino acids) encoded by the SNCA gene is the best known isoform of the synuclein protein family. Though its physiological role is still not fully clarified, there is growing experimental evidence for a causal role of α-synuclein in the so-called conformational-neurodegenerative diseases. Conformational changes in the structure of the native soluble protein form insoluble neurotoxic aggregates and finally contribute to the formation of inclusion Lewy-bodies and Lewy-neurites. Neurodegeneration first hits the olfactory system, the peripheral autonomic nervous system, the enteric nervous system and the dorsal vagal motoneurons. The middle stage of the disease hits the dopaminergic neurons of the substantia nigra; and the neocortex is affected only in the late stage of the disease. This precise order of neurodegeneration is not always valid, but increases the likelihood that Lewy-bodies and neurodegenaration spread to intact areas in a prion-like way. Prions are infectious proteins which do not contain nucleic acids and cause diseases because they form toxic aggregates and filaments by misfolding in a β-sheet-rich conformation. The misfolded protein behaves like a template inducing conformational change in the wild type proteins causing cross-reaction and leading to neurodegeneration. Later, the defective proteins may infect healthy nerve cells, thus neurodegeneration is extended. Growing experimental evidence shows that monomers and aggregates of α-synuclein are secreted via exocytosis from damaged nerve cells and taken up via endocytosis by healthy nerve cells furnishing evidence for the prion-like role of α-synuclein.

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Overview of systematic reviews.

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In rats, a selective inhibition for 3 weeks of monoamineoxydase (MAO) type B elicited by daily doses of pargyline (2.5 mumol/kg) or (-)-deprenyl (1 mumol/kg) attenuated the NE dependent stimulation of cortical adenylate cyclase and reduced the number of brain recognition sites for beta-adrenergic receptor ligands. Similar actions were not elicited by a comparable dose regimen of (+)-amphetamine. Hence the inhibition of MAO B mimicks responses that are typically elicited by antidepressants. The molecular nature of the mechanisms involved cannot be understood, however, these mechanisms may not be identical for pargyline and (-)-deprenyl because this drug but not pargyline increased the number of [3H]imipramine recognition sites. Even high daily doses of pargyline (100 mumol/kg, for 3 weeks) failed to change [3H]imipramine binding though they still down regulated beta-adrenergic recognition sites, the NE stimulation of adenylate cyclase and the Bmax of [3H]mianserin and [3H]spiroperidol binding.

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Two hundred patients at a median age of 63 years, receiving conventional levodopa therapy for 8 years, who had had Parkinson's disease for 10 years, tried a regimen of selegiline (L-deprenyl), a type B monoamine oxidase inhibitor, at a daily dose of 10 mg, for varying periods from less than 6 months to more than 24 months (28% over 24 months). Selegiline does improve parkinsonism during the initial 6 months to 12 to 24 months of combined therapy in one third to almost half of patients with an end-of-dose type of response to long-term levodopa therapy. However, even this particular class of patients is unable to maintain such an improvement by 36 months, much less by 48 months, from the start of the selegiline trial. About one quarter of poor responders to levodopa and those with random deterioration show improvement in their parkinsonian status in the first 6 months of the selegiline trial, but their conditions quickly deteriorate by 1 year. The predominant pattern of response to previous levodopa therapy and the severity of the total disability score at the initiation of the selegiline trial were the two variables that were predictive of risk of failure with the drug. No evidence suggested that selegiline decreases the excess mortality rate of Parkinson's disease above that achieved with the use of levodopa alone. Selegiline as an adjunctive agent to conventional levodopa therapy was not unduly impressive with regard to preventing progression of Parkinson's disease.

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Selegiline shows potential for the management of apathy following TBI. This provides further evidence that impaired dopaminergic processes are prominent in the genesis of these symptoms. However, these findings require confirmation in controlled studies.

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The SELEDO (from selegiline plus levodopa) study was carried out as a randomized, prospective, placebo-controlled, double- blind, multicenter long-term, 5-year trial to evaluate the possible advantages of combining selegiline and levodopa in the early treatment of Parkinson's disease. One-hundred-and-sixteen patients were randomized either to selegiline or placebo. Before starting the study medication, the levodopa dose was titrated to the individual requirements of each patient. The primary study end point (time when levodopa had to be increased by >50% of the titrated dose) was reached in 23 of 59 patients in the selegiline group and 26 of 48 patients in the placebo group. At the end of the 5 years' treatment period the rates derived from a life-table analysis were 50.4% in the selegiline group and 74.1% in the placebo group (P = 0.027, log-rank test). The median time to reach the primary end point was 4.9 years in the selegiline group and 2.6 years in the placebo group. In patients treated with selegiline, the mean levodopa dose changed only slightly over the 5 years of treatment compared to the initially titrated dose, but rose markedly in the placebo group, where the dose of levodopa had to be adjusted earlier than in the selegiline group. At the same time, the lower levodopa dosage in the selegiline group was accompanied by at least equal therapeutic efficacy (which is necessary for an unambiguous interpretation). Subgroup analyses showed greater benefit for selegiline treated) patients in the earlier stages. Long-term side effects appeared later in the selegiline group, although the difference was not significant. The early combination of selegiline and levodopa proved to be clearly superior to levodopa monotherapy.

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It appears that selegiline and rasagiline have comparable efficacy in improving Parkinsonian symptoms in patients with early stage disease.

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3,4-Methylenedioxymethamphetamine (MDMA)-induced serotonergic neurotoxicity was assessed in the striatum, hippocampus and frontal cortex of rats by using [3H]paroxetine binding to label serotonin (5-HT) uptake sites and 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) levels as markers of serotonergic function. NMDA (40 mg/kg) induced a significant decrease in both [3H]paroxetine binding Bmax and 5-HT and 5-HIAA levels 7 days after treatment. The monoamine oxidase-B inhibitor L-deprenyl (2 mg/kg) administered 30 min before MDMA blocked these decreases. MDMA (40 mg/kg) also maximally increased the formation of thiobarbituric acid reactive substances (an indicator of lipid peroxidation) 12 hr after treatment in all three brain regions studied. This increase in malondialdehyde formation was also blocked by pretreatment with L-deprenyl. Tryptophan hydroxylase (TPH) activity was also significantly reduced 18 hr after MDMA. L-Deprenyl reversed this decrease in TPH activity. Another experiment confirmed that a significant fraction of [3H]dopamine uptake into hippocampal synaptosomes was blocked by 500 nM fluoxetine, a selective 5-HT uptake inhibitor. These data suggest that the deamination by monoamine oxidase-B of excessive dopamine within the 5-HT terminal generates hydrogen peroxide that may lead to membrane lipid peroxidation, and perhaps other oxidative insults, resulting in selective 5-HT terminal degeneration subsequent to MDMA treatment.

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Selegiline is an irreversible inhibitor of monoamine oxidase B with trophic and neuroprotective effects. Because of evidence for decreased dopaminergic function during the withdrawal syndromes associated with opiates and other medications with potential for abuse, we investigated effects of treatment with selegiline on in vitro measures of dopamine efflux following opiate withdrawal. Treatment with 2.0 mg/kg/day of selegiline did not modify the severity of opiate withdrawal, as assessed by weight loss over the first 3 days of abstinence. Opiate withdrawal increased immobility in response to a forced warm water swim test performed during the second and third weeks of abstinence following the onset of withdrawal. Brain slices obtained from the nucleus accumbens of opiate-withdrawn animals immediately following swim stress testing displayed diminished efflux of tritiated dopamine after two in vitro exposures to cocaine or amphetamine. Cocaine increases neurotransmitter efflux through blockade of dopamine reuptake, while amphetamine augments efflux by stimulating release of dopamine from intracellular storage vesicles. Although slices from opiate withdrawal subjects showed decreases in efflux after in vitro treatment with these agents, no differences were observed after exposure to 4-aminopyridine, which increases neurotransmitter release by prolonging action potential duration. These findings indicate mechanisms of action that are specific for catecholamine neurotransmitter systems are important for demonstrating long-term changes in dopaminergic function following opiate withdrawal. Selegiline prevented decreases in the efflux of tritiated dopamine in slices obtained from opiate-withdrawn subjects. In addition, selegiline decreased withdrawal-induced immobility during warm water swim testing. In conclusion, treatment with selegiline can prevent long-term changes in stress-induced immobility and deficits in presynaptic dopaminergic function that occur following the opiate withdrawal syndrome.

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For several years there is controversy concerning the toxic potency of reaction products catalyzed by monoamine oxidase in neurodegenerative processes. There is uncertainty whether products of catecholamine oxidation are pathogenetically relevant factors for neuronal cell death in Parkinson's disease. To date products responsible for impairment of biochemical functions essential for cell viability are not yet identified, and the primary site of damage within the cell is unknown. Ammonia, aldehydes and hydrogen peroxide are formed via monoamine oxidase catalyzed oxidations of primary amines. But which of them, if any, is damaging to the cell? We discuss some aspects of the oxidative stress theory of cell degeneration in relation to toxicity of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and to monoamine oxidation. Furthermore, we consider possible functional relationships of mitochondrial electron transfer reactions, toxicity of MPTP and MAO activity.

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The cardiovascular responses to standing and head-up tilt were studied repeatedly in PD patients receiving selegiline and as the drug was withdrawn.

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To determine the possible impact of CYP2D6 polymorphism on the pharmacokinetics and pharmacodynamics of selegiline.

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The effects of L-deprenyl, a monoamine oxidase-B (MAO-B) inhibitor, on the concentrations of norepinephrine (NE), dopamine (DA), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), serotonin (5-hydroxytryptamine), and 5-hydroxyindoleacetic acid (5-HIAA) in medial basal hypothalamus (MBH), substantia nigra (SN), striatum (Str), and nucleus accumbens (NAc) of young (3 month) and old (21 month) male F344 rats were examined after a 7-day wash-out period following 1, 15, or 30 days of deprenyl treatment in young rats and a 9-day wash-out period after a 10-week deprenyl treatment in old rats. The brain areas were microdissected and the concentrations of neurotransmitters were measured by High Performance liquid chromatography with electrochemical detection (HPLC-EC). Deprenyl administration following the drug wash-out period increased the concentrations of DOPAC in the SN, Str, and in the NAc of young rats but it was decreased in the NAc of old rats. The concentration of HVA was lower in the Str of young deprenyl-treated rats, and in the Str and NAc of old deprenyl-treated rats, but it was higher in the SN of young deprenyl-treated rats. The concentration of 5-HIAA was increased in the MBH, SN, and in the NAc of young deprenyl-treated rats, but it was decreased in the Str and NAc of old deprenyl-treated rats. The concentration of NE was increased in the MBH, SN, Str, and in the NAc of young rats treated with deprenyl and in the MBH of old deprenyl-treated rats. The concentration of 5-HT was increased in the SN of young deprenyl-treated rats. The concentration of DA increased in the Str of both young and old deprenyl-treated rats. We concluded that a drug wash-out period after deprenyl treatment differentially affects the metabolism of catecholamines and indoleamine depending on the region of the brain and that this effect may be due to variation in the kinetics of MAO inhibition.

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Results from this double-blind, placebo-controlled clinical trial demonstrate that STS may have a modest, but statistically significant, antidepressant benefit compared with placebo and a similar safety profile compared with placebo in the absence of a tyramine-restricted diet.

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Effects of aging on brain dopaminergic system, e.g., neurotransmitter metabolism and different kinds of dopamine-dependent behaviour, were studied in mice of three inbred strains. Homovanillic acid concentrations in structures of both nigrostriatal (striatum) and mesolimbic (n. accumbens with tuberculum olfactorium) systems were found to be increased in the aged animals. Aged mice of the strains studied were characterized by decreased locomotor activity and stereotypic climbing; CC57Br mice, in contrast to A/He and C3H/He, demonstrated significantly diminished level of investigatory activity. However, genotypic differences in these kinds of behaviour were less pronounced in the aged animals in comparison to the young adults, but interstrain differences in swimming activity (Porsolt's "despair test") which was almost unchanged in aged mice, remained enough pronounced. In the aged mice postsynaptic dopamine receptor sensitivity, assessed after administration of a high dose of the mixed agonist apomorphine, was markedly decreased. Chronic treatment with deprenyl, a specific MAO-B inhibitor, produced a clear-cut genotype-dependent effect on investigatory activity in the aged animals. High level of this activity, characteristic for the young adults, was restored in CC57Br, in A/He it was elevated in comparison both with young and old untreated animals, and the same tendency was observed in C3H/He. This fact seems to reflect an interesting property of deprenyl to increase general adaptation in the aged organism, that might have valuable clinical implications.

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Past studies including our own have confirmed that chronic administration of deprenyl can prolong life spans of at least four different animal species. Pretreatment with the drug for several weeks increases activities of superoxide dismutase (SOD) and catalase (CAT) in selective brain regions. An up-regulation of antioxidant enzyme activities can also be induced in organs such as the heart, kidney, spleen, and adrenal gland, and all are accompanied by an increase in mRNA levels for SODs in these organs. The effect of deprenyl on enzyme activities has a dose-effect relationship of a typical inverted U shape. A similar inverted U shape also has emerged for the drug's effect on survival of animals. An apparent parallelism observed between these two effects of the drug seems to support our contention that the up-regulation of antioxidant enzymes is at least partially responsible for the life-prolonging effect on animals. Further, when a clinically applied dose of the drug for patients with Parkinson's disease was given to monkeys, SOD and CAT activities were increased in striatum of these monkeys, which suggests potential for the drug's applicability to humans. The drug was also found to increase concentrations of cytokines such as interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) in the above rat organs. Together with past reports demonstrating that deprenyl increases natural killer (NK) cell functions and interferon-gamma, and prevents the occurrence of malignant tumors in rodents and dogs, the mobilization of these humoral factors may therefore be included as possible mechanisms of action of deprenyl for its diverse antiaging and life-prolonging effects. The potentials of propargylamines, (-)deprenyl in particular, for human use as antiaging drugs remain worthy of exploration in the future.

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eldepryl drug classification 2017-04-12

The concept of neuroprotection relates to the fact that intervention may be able to interfere with the pathogenesis of neuronal cell death. Neuroprotective therapy may make it possible to delay disease progression or prevent the disease altogether. The pathophysiological mechanism of cell death in Parkinson's disease is unknown; however, hypotheses have been developed. The discovery that the toxin MPTP can cause Parkinson's disease both in humans and in animals strengthened the hypothesis that either exogenous or endogenous toxins may be involved in the mechanism of cell death in Parkinson's disease. The mechanism of MPTP toxicity has been elucidated, lending several possible mechanisms for therapeutic intervention in Parkinson's disease. Current data suggest that oxidative stress may play a prominent role buy eldepryl in the pathogenesis of Parkinson's disease. It is possible that the generation of free radicals leads to neuronal cell death. There is also evidence that mitochondrial damage may play a role in the pathogenesis of Parkinson's disease. Other theories of possible pathogenesis include excitotoxicity, disturbances of calcium homeostasis, immunological mechanisms, and infectious etiologies. The first agent to be tested as a candidate for neuroprotection was the MAO-B inhibitor deprenyl. Evidence is reviewed for and against the theory that this drug is neuroprotective.

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The major side effect with the use of first generation of non selective monoamine oxidase (MAO) inhibitors as neuropsychiatric drugs was what became known as the "cheese reaction". Namely, potentiation of sympathomimetic activity of ingested tyramine present in cheese and other food stuff, resulting from its ability to release noradrenaline, when prevented from metabolism by MAO. The identification of two forms of MAO, termed types A and B and their selective irreversible inhibitors resolved some of this problems. However irreversible MAO-A inhibitors continue to induce a cheese reaction, whereas MAO-B inhibitors at their selective dosage did not and led to introduction of L-deprenyl (selegiline) as an anti-Parkinson drug, since dopamine is equally well metabolized by both enzyme forms. The cheese reaction is a consequence of inhibition of MAO-A, the enzyme responsible for metabolism of noradrenaline and serotonin, located in peripheral adrenergic neurons. The consequence of these findings were the development of reversible MAO-A inhibitors (RIMA), moclobemide and brofaromin, as antidepressants and possible anti-Parkinson activity, with limited tyramine potentiation, since the amine can displace the inhibitor from its binding site on the enzyme. It has always been deemed a greater pharmacological advantage to inhibit both forms of the enzymes to get the full functional activities of the amine neurotransmitters, and without inducing a "cheese reaction". This was not possible until recently, with the development of the novel cholinesterase-brain selective MAO-AB inhibitor, TV3326 (N-propargyl-(3R)-aminoidnan-5-yl-ethyl methylcarbamate hemitartiate), a carbamate derivative of the irreversible MAO-B inhibitor anti-Parkinson drug, rasagiline. This drug is a brain selective MAO-A and B inhibitor, with little inhibition of liver and small intestine enzymes. buy eldepryl Pharmacologically it has limited tyramine potentiation, very similar to moclobemide and being a MAO-AB inhibitor it has the antidepressant, anti-Parkinson and anti-Alzheimer activities in the respective models used to develop such drugs.

cost of eldepryl 2016-08-07

To study the buy eldepryl development of freezing of gait in PD.

eldepryl dosage 2017-01-27

Astrocytes are likely to be a main locus for the metabolic bioactivation of the neurotoxicant 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). In this study, a detailed analysis of MPTP metabolism was conducted in primary cultures of mouse astrocytes. A constant rate of conversion of 1.22 nmol/mg of protein per hr was observed when astrocyte cultures were incubated in the presence of 250 microM MPTP for 4 days. Three metabolites were detected as products of this conversion: 1-methyl-4- buy eldepryl phenyl-2,3-dihydropyridinium ion (MPDP+), 1-methyl-4-phenylpyridinium ion (MPP+) and MPTP N-oxide. Production of MPP+ and MPTP N-oxide occurred at constant rates of 0.68 and 0.43 nmol/mg of protein per hr, respectively, whereas the level of MPDP+ remained quite stable and relatively low throughout the time of incubation. Both clorgyline, an inhibitor of monoamine oxidase (MAO) type A, and deprenyl, a MAO B inhibitor, blocked MPTP conversion to MPDP+ and MPP+; quantitative analysis of the effects of these two inhibitors revealed that MAO A and MAO B contribute to a similar extent to MPP+ production in astrocyte cultures. MAO inhibition did not result in an increased production of MPTP N-oxide and, in fact, the level of this metabolite was reduced markedly in the presence of 100 microM clorgyline. Formation of MPTP N-oxide was probably dependent upon the activity of the flavin-containing monooxygenase because: 1) it was blocked completely by thiobenzamide, a competitive substrate for this microsomal enzyme and 2) it was increased in the presence of n-octylamine, a known positive effector for flavin-containing monooxygenase.(ABSTRACT TRUNCATED AT 250 WORDS)

eldepryl medication 2015-08-03

Beliefs about smoking assessed prior to the quit attempt were not associated with cessation outcomes. Participants who quit smoking reported a reduction in expectations that smoking would reduce negative affect, boredom, and cravings, and facilitate social interactions, while participants who did not quit smoking reported an increase in Negative Social Impression beliefs. There were gender differences in beliefs related to Negative Affect Reduction, Negative Physical buy eldepryl Feelings, Social Facilitation, and Cravings and significant Gender X Smoking Status interactions for Health Risk and Weight Control beliefs. There were no significant effects of medication on expectancies.

eldepryl syrup 2015-11-14

Increasing age decreases spatial learning and memory. Spatial learning is coordinated with different brain regions. Since the oxidative damage may play a role in the aging process, including the associated cognitive decline, age-related impairment in spatial learning and memory may be alleviated by antioxidant treatment. The present study examined the effects of the monoamine oxidase B inhibitor L-deprenyl, alone and in combination with estradiol, on spatial memory using the Morris water maze and oxidant stress in buy eldepryl aged female rat brains. We demonstrated that co-administration of deprenyl and estradiol caused a synergistic effect on spatial memory. However, use of either deprenyl or estradiol alone increased antioxidant enzyme activities in brain and reduced lipid peroxidation. Therefore, positive effects of deprenyl and estradiol on spatial memory may occur due not only to their antioxidant activities but also to the different actions.

eldepryl drug interactions 2015-07-23

Treatment with levodopa and dopa decarboxylase inhibitor (arm 1) or levodopa and decarboxylase inhibitor in buy eldepryl combination with selegiline (arm 2).

buy eldepryl online 2017-12-25

For many years, visual hallucinations (VH) in idiopathic Parkinson's disease (PD) were thought to be a complication buy eldepryl of antiparkinsonian treatment. The cause of VH is now thought to be nerve-cell loss and Lewy-body pathology in the ventral-temporal regions of the brain. However, the use of VH as a clinical sign of PD has not been investigated.

eldepryl generic 2017-11-09

We considered all randomised or quasi randomised trials buy eldepryl that have evaluated any type of psychostimulants (versus a placebo or no treatment) in children or adults with proven myotonic dystrophy and hypersomnia.

eldepryl tablets 2017-02-09

In the mid-1980s, the treatment of Parkinson's disease was quite exclusively centered on dopatherapy and was focusing on dopamine systems and motor symptoms. A few dopamine agonists and a monoamine oxidase B inhibitor (selegiline) were used as adjuncts in advanced Parkinson's disease. In the early 2010s, levodopa remains the gold standard. New insights into the organization of the basal ganglia paved the way for deep brain stimulation, especially of the subthalamic nucleus, providing spectacular improvement of drug-refractory levodopa-induced motor complications. Novel dopamine agonists (pramipexole, ropinirole, rotigotine), catecholmethyltransferase inhibitors (entacapone), and monoamine oxidase B inhibitors (rasagiline) have also been developed to provide more continuous oral delivery of dopaminergic stimulation in order to improve motor outcomes. Using dopamine agonists early, before levodopa, proved to delay the onset of dyskinesia, although this is achieved at the price of potentially disabling daytime somnolence or impulse control disorders. The demonstration of an antidyskinetic effect of the glutamate antagonist amantadine opened the door for novel nondopaminergic approaches of Parkinson's disease therapy. More recently, nonmotor symptoms (depression, dementia, and psychosis) have been the focus of the first randomized controlled trials in this field. Despite therapeutic advances, Parkinson's disease continues to be a relentlessly buy eldepryl progressive disorder leading to severe disability. Neuroprotective interventions able to modify the progression of Parkinson's disease have stood out as a failed therapeutic goal over the last 2 decades, despite potentially encouraging results with compounds like rasagiline. Newer molecular targets, new animal models, novel clinical trial designs, and biomarkers to assess disease modification have created hope for future therapeutic interventions.

eldepryl dosage forms 2017-10-01

(-)-Deprenyl and rasagiline are classified as selective inhibitors of B-type MAO. The DATATOP study revealed that the administration of (-)-deprenyl to untreated buy eldepryl patients with Parkinson's disease (PD) significantly delays the need for levodopa therapy (Parkinson Study Group, 1989). Rasagiline was ineffective in this respect (Parkinson Study Group, 2002). The aim of this paper is to explain the reasoning behind the differentiation between (-)-deprenyl and rasagiline.

eldepryl drug 2017-12-28

Clinical Global Impressions scale and Nurses Observation Scale for Inpatient Evaluation at baseline and at weeks 6, buy eldepryl 12 and 24; Clock Drawing Test at baseline and 24 weeks, results of which were evaluated as normal or pathologic, and quantitatively on a modified 6-point scale; Sternberg's Memory Scanning test at baseline and at weeks 6, 12 and 24; Mini Mental State Examination, and electroencephalogram at baseline and 24 weeks; Structured Adverse Effects Rating Scale; physical, laboratory, hematological and electrocardiographic examinations at baseline and weeks 12 and 24.

eldepryl cost 2015-08-29

1. Deprenyl is metabolized by rat liver microsomes into methamphetamine (MAP), amphetamine (AP) and nor-deprenyl, and by lung and kidney microsomes into MAP. 2. Treatment of rats with phenobarbital (PB), but not 3-methyl-cholanthrene (3-MC), resulted in significant increases in hepatic metabolism of deprenyl to MAP and AP, and in a slight increase in the pulmonary metabolism of the drug to MAP. Neither treatment showed any effect on the renal metabolism of deprenyl. 3. Luvox Highest Dose The inhibitory effect of deprenyl on monoamine oxidase (MAO) B activity of liver was decreased and increased by pretreatment of rats with PB and SKF 525-A, respectively. However, inhibition by deprenyl of MAO-B activity of extrahepatic tissues was not affected by such treatments, except the lung where PB decreased the potency of the drug. 4. Sex differences in the hepatic metabolism of deprenyl to amphetamines were seen in all three strains of rats, Sprague-Dawley, Wistar and Donryu. However, no sex differences observed in the extrahepatic metabolism of deprenyl. 5. Strain differences were also seen in the metabolism of deprenyl, depending on the tissues and metabolites examined.

eldepryl buy 2015-03-25

(1) The reference treatment for Parkinson's disease is levodopa plus a peripheral dopadecarboxylase inhibitor (benserazide or carbidopa). (2) In 1996, selegiline, a type B MAOI marketed in France since 1988, saw its indications extended to cover single-agent therapy of early-stage Parkinson's disease, and in combination with levodopa, before onset of complications of levodopa therapy. The initial clinical file failed to show that selegiline had any benefit in these indications. (3) Now, in 2002, new data from trials involving hundreds of untreated patients show that selegiline postpones the need for levodopa therapy for a few months but fails to substantially alter the progression of Parkinson's disease. (4) A clinical trial and a retrospective epidemiological study of patients with advanced Parkinson's disease showed excess mortality on selegiline. (5) The side effects of selegiline are similar to those of other antiparkinsonian drugs and amphetamine. Notable side effects include cardiovascular problems (postural hypotension, atrial fibrillation and arterial hypertension). (6) Selegiline can cause a serotoninergic syndrome and arterial hypertension, so must Zovirax 200 Syrup not be combined with pethidine, tramadol, bupropion, sumatriptan, zolmitriptan or naratriptan. Concurrent treatment with serotonin reuptake inhibitor antidepressants should also be avoided. (7) Given the only moderate effects of selegiline in Parkinson's disease, and the possibility of a slight increase in mortality, there is no justification for prescribing this medication in patients with Parkinson's disease. (8) Whatever the stage of Parkinson's disease, there is no justification for starting patients on selegiline. Patients who are already taking selegiline should only continue to take it if they feel a clear benefit and are free from risk factors for early mortality, especially cardiovascular disease.

eldepryl order 2015-02-26

One hundred fifty-seven de novo PD patients were randomized in a double-blind, placebo-controlled study of 7 years' duration. In the monotherapy part Cymbalta 200 Mg , selegiline significantly delayed the initiation of levodopa therapy vs placebo. The authors now report the results from the combination part of the study, in which 140 patients received selegiline or placebo in addition to individually tailored levodopa therapy.

eldepryl reviews 2015-12-07

Complex pharmacological effect of l-deprenyl cannot be explained by its MAO-B inhibitory action only. In contrast to other parent MAO inhibitors (J-512, J-516, LK-63, U-1424) l-, and d-deprenyl inhibit the hypothalamic noradrenaline and striatal dopamine (DA) reuptake without influencing the uptake of serotonin, both in rat and in human brain. Long-term treatment 19 x 0.25 mg/kg or 0.5 mg/kg, sc with l-deprenyl elicits 37 +/- 2.8 and 43 +/- 3.2% inhibition, respectively, of DA reuptake capacity in the rat striatal cell-free homogenate. To compare the potencies of deprenyl isomers on DA and DOPAC levels of rat striatum drugs were given 0.25, 2 and 8 mg/kg ip and their effects measured 4 and 48 h after treatment. DA content was increased only by 8 mg/kg d-deprenyl 4 h after its injection, but DOPAC level was decreased 3 Diflucan Pills by both isomers. After 48 h, actions of d-deprenyl terminated but the effect of l-deprenyl was still present.

eldepryl medication dose 2016-02-10

Caring for the caregiver is a significant part of managing a patient with AD Zovirax Cream Cost . Many predictors of caregiver burden in AD have been identified. A number of measurement tools have been developed to assess caregiver burden in the research setting. A wide variety of interventions to reduce caregiver burden have been studied. These interventions range from education and support services to drug therapies. Most often these strategies have been studied individually; however, combining drug treatments with nonpharmacologic interventions may be the best approach to improve the quality of life for the caregiver of a patient with dementia and the care recipient. Most of the studies to date of drug therapy and caregiver burden have evaluated cholinesterase inhibitors. Other drug therapies that have been studied include memantine, antipsychotics, antidepressants, and selegiline. PRIMARY CONCLUSIONS AND CLINICAL APPLICATIONS: The pharmacist can play an important part in reducing the caregiver burden associated with AD. It is important to identify caregivers at risk for experiencing significant caregiver burden since the consequences of excess burden to the caregiver-and the care recipient-can be devastating. Among the many tasks of providing such care, caregivers are responsible for administering and managing medications. The difficulties associated with the care recipient's medications can be reduced through effective communication, education, and services available from a pharmacist. Pharmacists are probably the most accessible health care professional for the caregiver. Being able to provide accurate information about AD and its management is an important way to ease the burden of care. Finally, pharmacists can play a significant part in supporting the community in caring for the families of patients with Alzheimer's disease by volunteering with the local chapter of the Alzheimer's Association.

eldepryl dosing 2015-07-25

There was no significant difference in mortality between the bromocriptine and the levodopa arms (hazard ratio 1.15 [95% CI 0.90, 1.47]). Patients initially randomized to bromocriptine had slightly worse disability scores throughout follow-up. This difference was significant during the first years. Patients in the bromocriptine arm returned to pretreatment disability levels one year earlier than those in the levodopa arm. Patients randomized to bromocriptine had a significantly lower incidence of Coumadin 20 Mg dyskinesias than those randomized to levodopa (rate ratio 0.73 [95% CI 0.57, 0.93]). However, this difference was not significant when only moderate to severe dyskinesias were considered. Patients in the bromocriptine arm had slightly lower rates of dystonias and on-off fluctuations, but moderate and severe forms were equally frequent in both arms.

eldepryl and alcohol 2017-05-15

There have been many claims that l-deprenyl may have distinct properties in slowing and perhaps even in reversing the progression of Parkinson's disease and other neurodegenerative conditions. This Celexa Brand Name article will consider the paucity of evidence that such is the case in humans and the more detailed results from studies with experimental animals indicating that deprenyl may indeed express such a property. The conflicting data on its mechanism of action are considered and the concept that it may function to enhance neuronal fitness is advanced as an alternative to the neuroprotection and neurorescue hypotheses. Possible lines of experimental development that would help resolve some of the many unanswered questions regarding l-deprenyl function are outlined.

eldepryl generic name 2017-03-04

Chronic treatment with L-deprenyl increases both mean and maximum life span and improves cognitive functions in the aged rat. The present study was designed to evaluate whether long-term treatment with L-deprenyl at a dosage not inhibiting the monoamine oxidase-B (MAO-B) (1.25 mg/kg/day) or inhibiting the enzyme activity (5 mg/kg/day) had any effect on the age-dependent microanatomical changes in the rat hippocampus. The hippocampus was chosen in view of its key role in learning and memory functions. Treatment with L-deprenyl started at 19 months and lasted Voltaren Dosage 75mg until the 24th month of age. Age-matched untreated rats were used as a control, whereas 11-month-old rats were used as an adult reference group. The number of nerve cell and glial fibrillary acidic protein-immunoreactive astrocyte profiles in the CA1 and CA3 fields of the hippocampus and in the dentate gyrus was decreased and increased, respectively in aged compared with adult rats. Treatment with 5 mg/kg/day, but not with 1.25 mg/kg/day L-deprenyl increased the number of neuronal profiles and decreased the number of astrocytes in the hippocampus of aged rats. The density of zinc stores in the associative intrahippocampal pathway of mossy fibres, which was decreased in aged animals, was increased after treatment with the two doses of L-deprenyl. Lipofuscin accumulation within the cytoplasm of pyramidal neurons of the hippocampus was reduced dose dependently by L-deprenyl treatment. These results suggest that long-term treatment with L-deprenyl is able to counter the expression of age-dependent microanatomical changes in the rat hippocampus. These effects seem only partially correlated with the MAO-B inhibitory activity of L-deprenyl.

eldepryl drug classification 2017-08-12

Selegiline (L-deprenyl) is a selective monoamine oxidase B (MAO-B) inhibitor Protonix Reflux Medication used in the treatment of Parkinson's disease. In addition, it is thought to rescue neurons with a loss of target-derived trophic support. Several mechanisms have been proposed to explain these phenomena, such as the production of neurotrophic actions through astrocyte activation, reduction of free radical production, or the presence of antiapoptotic properties. The aim of this study was to investigate whether the systemic administration of selegiline facilitates recovery after a cerebral infarction in humans.

eldepryl 5 mg 2017-01-04

The effect of chronic treatment of aged rats with nomifensine has been studied in the rat nigrostriatal dopaminergic system. The rat substantia nigra suffers an oxidative damage during aging that results in both an increase in carbonyl groups of its total proteins and the oxidative inactivation of tyrosine hydroxylase (TH) enzyme, which are partially reversed by chronic treatment with deprenyl. Different mechanisms may account for this effect, including inhibition of the high-affinity dopamine uptake system. We treated aged rats chronically with nomifensine for 2 months and found some significant effects. Nomifensine treatment significantly increased TH enzyme amount in substantia nigra (39.2%), which was accompanied by a significant increase in TH enzyme activity (47.8%). However, these effects were not observed in the terminal field (striatum). As a further step we quantified the oxidative level of proteins by measuring the number of carbonyl groups coupled either to total proteins or specifically to TH enzyme. The proteins of aged rat substantia nigra showed a significant increase of carbonyl groups following nomifensine treatment. The number of carbonyl groups coupled to nigral TH enzyme also increased in the nomifensine-treated animals. However, this increase was lower than that found in the total homogenate proteins. All these results show that the oxidative damage produced during aging in tyrosine hydroxylase enzyme and total proteins is not reduced by nomifensine treatment. On the contrary, the nomifensine treatment increased the oxidative damage to proteins. These results suggest the capability of deprenyl to induce TH enzyme could be due to inhibition of the high-affinity dopamine uptake system, but its ability to protect against oxidative damage is not produced by this mechanism.

cost of eldepryl 2016-01-28

We have shown recently that selegiline exerts a cardiac neuroprotective effect in chronic heart failure. Since selegiline has an antioxidant antiapoptotic effect, we proposed to determine whether selegiline attenuates cardiac oxidative stress and myocyte apoptosis in chronic heart failure by modulating Bcl-2 and Bax protein expression, and whether the effects are associated with the improvement of cardiac function. Rabbits with rapid cardiac pacing (360 beats/min) and sham operation without pacing were randomized to receive oral selegiline (1 mg/day) or placebo for 8 weeks. Echocardiography was used to measure left ventricular fractional shortening. After 8 weeks of treatment, animals were studied for arterial norepinephrine and left ventricular systolic function (fractional shortening and dP/dt), and were then sacrificed for measuring the stable oxidative product of myocardial mitochondrial DNA (mtDNA) 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxo-dG), myocyte apoptosis by monoclonal antibody to single stranded DNA, and Bcl-2 and Bax protein expression by Western blot and immunohistochemistry. Rapid cardiac pacing increased plasma norepinephrine, cardiac oxidative stress and myocyte apoptosis, reduced Bcl-2 and the Bcl-2 to Bax ratio. These changes were associated with decreased left ventricular fractional shortening and dP/dt. Selegiline treatment in chronic heart failure animals reduced plasma norepinephrine, cardiac oxidative stress and myocyte apoptosis, prevented the changes of Bcl-2 and Bcl-2 to Bax ratio, and improved left ventricular fractional shortening and dP/dt. The findings suggest that the reduction by selegiline of myocyte apoptosis is related to the decrease of cardiac oxidative stress and the modulation of apoptotic and antiapoptotic proteins. The antioxidant antiapoptotic effects of selegiline are potentially beneficial in the improvement of cardiac function in chronic heart failure.

eldepryl dosage 2015-04-11

Human brain total superoxide dismutase activity (SOD) was assayed in the presence of increasing concentrations of neuroprotectives. Superoxide-dependent nitrobluetetrazolium (NBT) reduction served as control for direct radical interaction of these substances. High concentrations of the dopamimetic substances L-DOPA slightly and the monoamine oxidase B inhibitor selegiline more effectively inhibit SOD activity. The MAO-B inhibitor RO 16-6491 (N-(2-aminoethyl)-4-chlorobenzamide hydrochloride) has no effect on SOD enzyme activity. Reduced glutathione stimulates SOD activity. Moreover it exhibits slight activity in scavenging radicals in vitro. Oxidized glutathione and vitamin E are unable to do so. Ascorbic acid mimics the activity of reduced glutathione, but directly interacts with NBT reduction. Thioctic acid shows no effect on SOD activity but stimulates superoxide-dependent NBT reduction. The Ginkgo biloba extract EGb 761 is highly active in inhibiting superoxide-dependent NBT reduction as well as SOD activity.

eldepryl medication 2017-11-27

To perform a clinical trial of selegiline in 25 patients with chronic fatigue syndrome (CFS) where patients were told they would receive placebo or active agent at different times during the 6-week trial. We chose selegiline, a specific monoamine oxidase (MAO) B receptor inhibitor, because a prior trial of lowdose phenelzine, a nonspecific MAO inhibitor, showed a small but significant therapeutic effect.

eldepryl syrup 2017-10-24

The author reviews the various strategies for treatment of Parkinson's disease by modern drugs. Either levodopa or a levodopa agonist is recommended for treatment of early Parkinson's disease. For long-term treatment, a combination of levodopa and levodopa agonist is preferable, since combined treatment appears to cause fewer side effects and motor fluctuations than does high dose monotherapy. Selegeline may be added, both in initial and long-term treatment. However, it is still uncertain whether selegeline acts only as a dopamine agonist, or also has a neuroprotective effect.