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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.

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Camptocormia in Parkinson's disease (PD) is unresponsive to various therapies and induced difficulties in their day-to-day life.

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A disturbance of the autonomic nervous system (ANS) in narcolepsy has been suggested, based on abnormalities on pupillometry, ejaculatory and cardiovascular function. The ANS function was studied by measuring the variation in the heart rate and blood pressure during provocations, using the following tests: deep breathing test, Valsalva test and Orthostatic test for heart rate reactivity measurements, and Orthostatic test for blood pressure control. Each test session gave seven variables, and these were compared to age-adjusted reference values in healthy normals. In 22 unmedicated narcoleptics (median age 50.5 y, range 18-70 y) the results did not differ from these. Seventeen of the patients were included in a controlled stimulant medication trial (selegiline 10-40 mg daily), and they showed no significant changes in the ANS variables except for a dose-dependent rise in heart ratio (placebo 1.32+/-1-0.13 and 40 mg 1.14+/-0.05; mean+/-SD) and a decrease in systolic blood pressure (placebo 5.8+/-9.7 and 40 mg 30.1+/-21.5 mmHg) on Orthostatic test. Although blood pressure decreases >/=30 mmHg (maximally 72 mmHg) occurred in 9 patients, they were asymptomatic. These changes are considered primarily to reflect the known characteristic of monoamine oxidase inhibitors to cause postural hypotonia. Abnormalities using these methods were not found, thus supporting the view that cardiovascular reflex abnormalities would be characteristic of narcolepsy.

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Newly introduced dopamine agonists, such as ropinirole, may offer advantages compared to such older drugs as bromocriptine in patients with advanced Parkinson's disease (PD) with response oscillations or waning efficacy. Dose equivalence of these two drugs, however, has not been well established, which may complicate switching in clinical practice. In 23 such patients with advanced PD no longer satisfactorily responsive to prolonged bromocriptine therapy (mean dose: 18.9 +/- 6.5 mg/d), we prospectively switched the medication to ropinirole administered at three different dose-ratios (5:1, 3:1, and 2:1), increased at monthly intervals. Selegiline remained unmodified in all 17 patients receiving this medication. A dose-ratio of bromocriptine to ropinirole of close to 2:1 (1.87; mean ropinirole dose: 10.1 +/- 2.5 mg/d) was the only dose that significantly reduced mean motor Unified Parkinson's Disease Rating Scale (UPDRS) scores ( p = 0.030, analysis of variance). Individually considered, however, four patients (21%) scored worse even at this dose-ratio when compared to baseline assessment on bromocriptine. "Off" time was reduced by 57.3% in fluctuating patients, and the dyskinesia score decreased by 53.8%, although the changes were not statistically significant. Higher bromocriptine to ropinirole dose ratios (i.e., 5:1 and 3:1) resulted in "off"-time increases in half of the patients with fluctuations, and two previously stable patients developed a wearing-off effect and one other patient experienced off-time dystonia. One patient developed dose-dependent dopaminomimetic psychotic symptoms with ropinirole. In conclusion, "off"-time motor scores and possibly "off"-time duration, and severity of dyskinesias in patients with advanced PD with prolonged bromocriptine therapy may improve in a majority of cases by switching to ropinirole, provided that the latter drug is administered at a dose ratio of 2:1 compared to bromocriptine. Higher dose ratios are often ineffective or may even cause a clinical worsening of symptoms in some patients.

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To determine whether adding orally disintegrating selegiline (ODS) while decreasing dopamine agonist (DA) dosages would reduce DA-related adverse effects (AEs) of excessive daytime sleepiness (EDS), pedal edema, hallucinations, and impulse control disorders (ICDs) without compromising efficacy in Parkinson disease (PD) patients.

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Studies were designed to evaluate specificity of the transmitter amines serotonin (5-hydroxytryptamine, 5-HT) and dopamine (DA), as well as the trace amines p-tyramine (p-TA) and beta-phenylethylamine (PEA) for types A and B monoamine oxidase (MAO) in rat striatum. 5-HT was found to be a specific substrate for the type A enzyme. However, the specificity of PEA for the type B enzyme was found to be concentration-dependent. When low concentrations of PEA and 5-HT were used to measure type B and type A activities, respectively, both clorgyline and deprenyl were highly selective for the sensitive form of MAO in vivo. However, as the concentration of PEA was increased, the type B inhibitor deprenyl became less effective in preventing deamination of PEA. Conversely, the type A inhibitor clorgyline became more effective in this regard. Kinetic analysis following selective in vivo inhibition showed PEA deamination by both forms of MAO with a 13-fold greater affinity for the type B enzyme. In vivo dose-response curves obtained with the common substrates DA and p-TA showed approximately 20% deamination by the B enzyme. Kinetic values for DA and p-TA deamination in in vivo-treated tissue possessing only type A or type B MAO activity, revealed a 2.5-fold greater affinity for the type A enzyme. These studies show the importance of concentration on substrate specificity in striatal tissue. The results obtained characterize the common substrate properties of DA and p-TA as well as of PEA in rat striatum. In addition, the presence of regional specificity for 5-HT deamination by only type A MAO is demonstrated.

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Murine P19 embryonal carcinoma (EC) cells are convenient to differentiate into all germ layer derivatives. One of the advantages of P19 cells is that the exogenous DNA can be easily inserted into them. Here, at the first part of this study, we generated stable GFP-expressing P19 cells (P19-GFP(+)). FACS and western-blot analysis confirmed stable expression of GFP in the cells. We previously demonstrated the efficient induction of neuronal differentiation from mouse ES and EC cells by application of a neuroprotective drug, selegiline In the second part of this study selegiline was used to induce differentiation of P19-GFP(+) into stable GFP-expressing neuron-like cells. Cresyl violet staining confirmed neuronal morphology of the differentiated cells. Furthermore, real-time PCR and immunoflourescence approved the expression of neuron specific markers. P19-GFP(+) cells were able to survive, migrate and integrated into host tissues when transplanted to developing chick embryo CNS. The obtained live GFP-expressing cells can be used as an abundant source of developmentally pluripotent material for transplantation studies, investigating the cellular and molecular aspects of early differentiation.

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In vivo microdialysis was used to concurrently measure the behavioral and caudate dopamine (DA) responses to the alleged irreversible type B monoamine oxidase inhibitor deprenyl. The effects were contrasted to those of the type A monoamine oxidase inhibitor, clorgyline. Consistent with its effects as an irreversible monoamine oxidase inhibitor, clorgyline produced an increase in DA concentration that remained elevated for at least 6 h. In contrast, the deprenyl-induced elevation in DA concentration occurred more rapidly, achieved a higher peak response, and then returned to baseline within 2 h following drug administration. The two drugs also produced distinctive changes in DA metabolite levels. Whereas the pattern of clorgyline-induced effects were consistent with irreversible monoamine oxidase inhibition, deprenyl produced an amphetamine-like response profile. Further, deprenyl but not clorgyline significantly increased locomotor activity. These results suggest that deprenyl does not augment caudate DA levels through monoamine oxidase inhibition. Rather, the pattern of its effects on caudate DA dynamics and behavior supports previous evidence that deprenyl produces its effects through its metabolism to amphetamine-like substances.

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To perform a secondary analysis of NET-PD LS1 to determine if longer duration of MAO-B inhibitor exposure was associated with less clinical decline.

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Trophic effects of the neuroprotective agent selegiline on cultured dopaminergic neurons were investigated and compared with the effects produced by brain derived neurotrophic factor (BDNF). Both treatments increased the total length of TH-positive neurites, but selegiline increased the average length of neuritic branches, whereas BDNF increased the formation of new branches. This trophic effect of selegiline may contribute to its action in neurodegenerative disease treatment.

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Selegiline delayed significantly the need to start levodopa in early PD. After a 2-month washout period (before the start of levodopa therapy) no significant symptomatic effect of selegiline was seen in comparison with the placebo group, supporting the concept of neuroprotective properties of the drug.

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Parkinson's disease is characterized by a severe loss of dopaminergic neurons resulting in a range of motor deficits. The neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is known to cause a similar loss of dopaminergic neurons in the human midbrain with corresponding Parkinsonian symptoms. Several animal species have also shown sensitivity to MPTP, including primates, mice, goldfish, and, most recently, zebrafish. This study demonstrates that the effect of MPTP on dopaminergic neurons in zebrafish larvae is mediated by the same pathways that have been demonstrated in mammalian species. MPTP-induced neurodegeneration was prevented by co-incubation with either the monoamine oxidase-B (MAO-B) inhibitor l-deprenyl or the dopamine transporter (DAT) inhibitor nomifensine. Furthermore, targeted inactivation of the DAT gene by antisense morpholinos also protected neurons from MPTP damage. Thus, the mechanism for MPTP-induced dopaminergic neuron toxicity in mammals is conserved in zebrafish larvae. Effects on swimming behavior and touch response that result from MPTP damage are partially ameliorated by both l-deprenyl and DAT knockdown.

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We are not confident that crossover studies are appropriate for this participant group. Sildenafil may be a useful option in the treatment of antipsychotic-induced sexual dysfunction in men with schizophrenia, but this conclusion is based only on one small short trial. Further well designed, conducted and reported trials are urgently needed.

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A solution of selegiline hydrochloride reference standard, which contained no detectable impurities at the time of its preparation, was found by HPLC to contain a trace of a compound at the locus of methamphetamine when analyzed after 1 year. Heating selegiline solutions at pH 7 and 105 degrees C produced methamphetamine as the major product at a rate which closely followed the first-order rate equation. Using only these data and worst-case assumptions, rate constants were estimated at various temperatures; the activation energy was estimated to be about 25 kcal, and the stability-indicating validity of the assay used was reaffirmed. Selegiline undergoes degradation at a negligibly slow rate.

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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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The combined treatment of deprenyl and gliclazide may contribute to the control of the physiopathological mechanisms underlying both the process of aging and type 2 diabetes by reducing oxidant stress and DNA damage, improving antioxidant status, and increasing survival, and may have implications for further clinical studies.

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Effects of a selective monoamine oxidase (MAO)--A inhibitor, clorgyline, a selective MAO-B inhibitor, deprenyl, and a non-selective MAO inhibitor, nialamide, were investigated on footshock-induced aggression (FIA) in paired rats. The doses and pretreatment times of the inhibitors used were based on an earlier reported in vivo dose-response and time-course study. In addition, apomorphine, a dopaminergic receptor agonist, and beta-phenylethylamine, a preferred substrate for MAO-B, were also used to garner corroborative evidence. The results of the study indicate that selective MAO-A inhibitors are likely to attenuate FIA by augmenting central serotonergic activity, while selective MAO-B inhibitors accentuate the behaviour by facilitating dopaminergic activity. A permissive role for noradrenaline could not be delineated by the available data.

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Using a fragment-based drug design strategy, two biomedical interesting fragments, resveratrol and coumarin were linked to design a series of novel human monoamine oxidase (hMAO) inhibitors with a scaffold of 3-((E)-3-(2-((E)-styryl)phenyl)acryloyl)-2H-chromen-2-one, which demonstrated a very interesting selectivity profile against hMAO-A and hMAO-B: some compounds with this scaffold are selective hMAO-A inhibitors, whereas some are selective hMAO-B inhibitors. The small changes in the substituents of the coumarin moiety led to this interesting selectivity profile. The most potent selective hMAO-B inhibitor D7 has a selectivity ratio of 20.93, with an IC₅₀ value of 2.78 μM, similar or better than selegiline (IC₅₀ = 2.89 μM), a selective hMAO-B inhibitor currently in the market for the treatment of Parkinson's disease. Our modeling study indicates that Tyr 326 of hMAO-B (or corresponded Ile 335 of hMAO-A) may be the determinant for the specificity of these compounds. The selectivity profile of compounds reported herein suggests that we can further develop both selective hMAO-A and hMAO-B inhibitors based on this novel scaffold.

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Monoamine oxidase specific activities against PEA and 5-HT have been measured in mitochondria isolated from early embryos of Bufo bufo. During the early development up to the neural fold stage, MAO activity undergoes a continuous decrease that is more evident when PEA is used as the substrate. The inhibition patterns of deprenyl and clorgyline demonstrate that, at the neural fold stage, both type A and B MAO are present. Both in eggs and embryos MAO type A activity appears slightly more sensitive to the inhibitory effect of various concentrations (0.1-2 M) of the denaturing agent urea.

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(-)Deprenyl (Selegiline), the N-propargyl analogue of (-)methamphetamine, is the only drug in clinical case which, by enhancing the impulse propagation mediated release of noradrenaline and dopamine in the brain (catecholaminergic activity enhancer, CAE, effect), keeps in small doses without side-effects the catecholaminergic brain system on a higher activity level. (-)Deprenyl stimulates the catecholaminergic neurons selectively in the brain because, in contrast to PEA and the amphetamines which induce the continuous release of noradrenaline and dopamine from their intraneuronal stores, (-)deprenyl is devoid of this property. It is due to the CAE effect that a) the maintenance of rats on (-)deprenyl during the postdevelopmental phase of their life slows the age-related decline of sexual and learning performances and prolongs life significantly; b) patients with early, untreated Parkinson's disease maintained on (-)deprenyl need levodopa significantly later than their placebo-treated peers, and when on levodopa plus (-)deprenyl, they live significantly longer than patients on levodopa alone; and c) in patients with moderately severe impairment from Alzheimer's disease, treatment with (-)deprenyl slows the progression of the disease. It is reasonable to expect that a prophylactic low dose administration of a safe catecholaminergic activity enhancer substance during the postdevelopmental phase of life will slow the age-related decline of behavioral performances, delay natural death and decrease susceptibility to Parkinson's disease and Alzheimer's disease.

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Preclinical studies indicate that selegiline (deprenyl), frequently used in some neurodegenerative diseases, exert protective effects on central nervous system neurons of individuals exposed to social isolation (SI). Furthermore, it has been suggested that SI produces neuronal dysfunction due in part to an excessive intracellular Ca(2+) overload. Since the main intracellular Ca(2+) buffering mechanism involves changes in the calcium-binding protein calbindin-D28k (CB), and that CB neuronal expression can increase in response to Ca(2+) transients, we hypothesized that chronic selegiline administration in early socially isolated animals could minimize cell CB expression as an indirect indicator of protective mechanism against Ca(2+) overload. In the present study male rats were weaned at postnatal day 21 (P21) and randomly assigned to social deprivation (SI) or control (SC) environments for 30 days (P21-51). SI animals were further subdivided in two experimental groups: socially deprived-saline (SI-SAL) and socially isolated-selegiline (SI-SEL) for additional 30 days (P52-82). Medial frontal CB immunoreactivity (CB-ir) neurons were quantitatively and qualitatively analyzed. The results obtained indicate that neocortical cells of adult rats submitted to early SI show a significant increase in the number of CB-ir neurons per cortical field, while selegiline treatment significantly reduces this parameter.

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Various doses of apomorphine, deprenyl, and yohimbine were administered to old (20-26 years) rhesus males that had been sexually active when younger and to younger (6-17 years) males that were characteristically sexually sluggish. These neuropharmacological agents have been reported to increase sexual behavior in male rats. In Experiment 1, 10 old intact rhesus males were tested after injection of vehicle and apomorphine, and 6 old testosterone-treated castrated males were tested after treatment with deprenyl and yohimbine and the vehicles for each drug. In experiment 2, the 5 younger males were tested after treatment with each of the drugs and with the vehicles for each drug. There were a few minor changes in behavior associated with certain doses of each of the drugs and as many depressive as facilitative effects on sexual behavior. This suggests that there are basic differences between rats and rhesus macaques in the systems mediating sexual behavior.

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1. Retinal dystrophies (RD) comprise a group of clinically and genetically heterogeneous retinal disorders, which typically result in the degeneration of photoreceptors followed by the impairment or loss of vision. Although age-related macular degeneration (AMD) and retinitis pigmentosa (RP) are among the most common forms of RD, currently, there is no effective treatment for either disorder. 2. Recently, abnormal protein accumulation and aggregation due to protein misfolding and proteasome inhibition have been implicated in the pathogenesis of RD. In this paper we describe effects of several factors on protein aggregation and survival of photoreceptor cells. 3. Expression of rhodopsin carrying P23H mutation causes its accumulation in intracellular inclusion bodies in a perinuclear area of photoreceptor cells. beta- and gamma-synucleins and heat shock protein Hsp-70, but not alpha-synuclein, protect cultured ocular cells from mutant opsin accumulation. This effect might be explained by their chaperonic activity. 4. Knock-out of alpha- and gamma-synucleins does not affect gross retinal morphology, but induces tyrosine hydroxylase in the inner prexiform layer of the retina. Selegiline-a monoamine oxidase inhibitor used for the treatment of Parkinson's disease, reduces apoptosis and increases viability in cultured retinal pigment epithelium cells (APRE-19). 5. These results suggest that chaperones and selegiline may be considered promising candidates for the protection of ocular cells from the accumulation of misfolded and aggregated proteins.

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There was no beneficial effect of tocopherol or any interaction between tocopherol and deprenyl. The beneficial effects of deprenyl, which occurred largely during the first 12 months of treatment, remained strong and significantly delayed the onset of disability requiring levodopa therapy (hazard ratio, 0.50; 95 percent confidence interval, 0.41 to 0.62; P < 0.001). The difference in the estimated median time to the end point was about nine months. The ratings for Parkinson's disease improved during the first three months of deprenyl treatment; the motor performance of deprenyl-treated patients worsened after the treatments were withdrawn.

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Inhibition of monoamine oxidase type B (MAO-B) activity in the brain is a putative strategy for the treatment of Alzheimer's disease (AD). We performed a dose-selection and validation study of a novel, reversible MAO-B inhibitor, EVT 301. Sixteen healthy volunteers received selegiline (10 mg) or EVT 301 (25, 75, or 150 mg) daily for 7-8 days, and four subjects with AD received 75 mg of EVT 301. MAO-B occupancy in the brain was assessed using positron emission tomography (PET) with [11C]-L-deprenyl-D2. EVT 301 was found to dose-dependently occupy MAO-B in the human brain, with occupancy ranging from 58-78% at a dose of 25 mg to 73-90% at a dose of 150 mg. The corresponding occupancy after selegiline was 77-92%. Determination of MAO-B inhibition in blood platelets underestimated the actual brain occupancy achieved with EVT 301. A daily EVT 301 dose of 75 or 150 mg appears suitable for clinical efficacy studies in patients with AD.

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Optimal treatment of primary negative symptoms is important because their presence is associated with poor outcome.

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The treatment of Parkinson's disease for most patients entails long term exposure to multiple agents, including anticholinergics, levodopa, amantadine, dopamine receptor agonists, catechol-O-methyltransferase inhibitors, selegiline (deprenyl) and clozapine. Patients with Parkinson's disease require medication for the control of the motor symptoms of their condition, for related medical or psychiatric symptoms of the disorder, and for concurrent medical problems, such as hypertension or cardiac disease.All these agents may cause adverse effects. There is a potential for drug-drug interactions between different antiparkinsonian agents and between antiparkinsonian medication and the other drugs a patient may be taking. Clinicians caring for patients with Parkinson's disease must be knowledgable about the potential adverse effects and drug interactions of an expanding array of medications for this condition.

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We extracted data in duplicate on the type of study population, the nature of the drug therapy, the outcome measures, method of randomisation, and completeness of follow-up. The main outcome measure was abstinence from smoking after at least six months follow-up in patients smoking at baseline. We used the most rigorous definition of abstinence for each trial, and biochemically validated rates if available. Where appropriate, we performed meta-analysis using a fixed effects model.

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A rate of utilization of 4-phenyl piperidine and its 12 derivatives by brain monoamine oxidase (MAO) was studied as compared with typical neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The enzyme was isolated from P2 synaptosomal fraction of brain corpus striatum of Sprague-Dawley rats. 10 drugs were oxidized in the MAO-catalyzed reaction with the rate close or similar to the MPTP oxidation while 6 of them exhibited the neurotoxic effect. Analysis of MAO inhibition, using 1 microM of chlorgyline and/or deprenyl, enabled to evaluate the contribution of MAO-A and MAO-B forms to utilization of 1 mM content of the substances studied. MAO-B was shown to oxidize preferably the drugs radicals of which were substituted at 3rd position of the piperidine ring, while MAO-A preferred the derivatives with radical substitution at 4th position. The rate of substrate oxidation was decreased distinctly after introduction of complete substituents into the 3rd and 4th positions of the nitrogenous heterocycle; at the same time, presence of cyclic fluorine-containing structures increased the rate of utilization, similar to that of MPTP oxidation. Derivatives of 4-phenyl piperidine, which contained in a number of drugs, were oxidized in the MAO-catalyzed reactions and might exhibit direct- or side-neurotoxic effects.

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eldepryl medication dose 2016-05-01

The primary aim of this study was to determine the safety buy eldepryl and efficacy of the monoamine oxidase-B (MAO-B) inhibitor selegiline hydrochloride (SEL, l-Deprenyl; Eldepryl) as an aid for smoking cessation in cigarette smokers.

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Our high buy eldepryl -throughput investigation identified monoamine oxidase-B, monoamine oxidase-A and angiotensin converting enzyme as potential targets for d-deprenyl. Further competitive [(3)H]d-deprenyl binding studies with specific inhibitors identified monoamine oxidase-B as the major binding site. No evident high-affinity hits were identified among G-protein coupled receptors.

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1. The effectiveness and tolerability of deprenyl as an adjunct in the therapy of parkinsonism was studied in a double-blind trial comprising 30 de novo patients. 2. Two thirds of the cases that could be evaluated showed a statistically significant improvement while on adjuvant deprenyl therapy. 3. The improvements are shown in the replugging test, a subtest of the Motor Performance Test, and on the Columbia University Rating Scale. 4. There is no statistically significant correlation between improvement of motor response and depression. 5. Deprenyl seems to be less effective in patients with low contents of HIAA and HVA buy eldepryl in the cerebrospinal fluid.

eldepryl generic 2015-09-08

To determine the optimum treatment for early buy eldepryl Parkinson's disease.

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In about 2/3 of the cases studied (152 patients), the combination of deprenyl and the substitution-therapy has a favourable effect as it tends to normalize buy eldepryl motor activity. Although the administering of deprenyl renders neither L-Dopa nor the decarboxylase inhibitor superfluous, their side effects can be slightly reduced as their dose is reduced. Therefore it is advised to give all patients a trial with this drug.

eldepryl 5 mg 2017-11-03

Aromatic L-amino acid decarboxylase (AADC) deficiency results in an impaired synthesis of catecholamines and serotonin, and has been reported only in two buy eldepryl middle eastern families. We report on a European family with an affected child. The child showed the characteristic clinical picture of an extrapyramidal movement disorder, oculogyric crises and vegetative symptoms seen in the three patients described previously. Treatment with a combination of the AADC cofactor pyridoxine, the monoamine oxidase B inhibitor selegiline and bromocriptine was started during the fifth year of life and showed only a moderate clinical improvement in contrast to patients who have been treated since the first year of life.

eldepryl dosage 2016-03-09

Psychosis arises with considerable frequency in a number of neurologic conditions. The treatment of such patients is often challenging, as many of the treatments for psychosis pose some risk of worsening the underlying neurologic condition. Although psychosis may emerge in the context of any neurologic condition that sufficiently disrupts the functioning of or connections between limbic, paralimbic, frontal, subcortical areas mediating complex sensory perception, interpretation, and thought or language organization, secondary psychoses are most often encountered in patients with Alzheimer's disease (Parkinson's disease receives dopaminomimetic therapies) and epilepsy. Psychosis, and particularly delusions and visual hallucinations, may arise buy eldepryl in Alzheimer's disease. Based on the available literature, the first-line therapy for this problem is risperidone 0.5 to 3 mg per day. If this treatment proves unsuccessful, low-dose haloperidol or olanzapine should be considered next. If these treatments prove unsuccessful, quetiapine should then be considered. Finally, clozapine may be useful for treatment-refractory psychosis due to Alzheimer's disease, but due caution is warranted given its considerable anticholinergic properties and potential for worsening cognition in these patients. Although disease-emergent psychosis (paranoid delusions and visual hallucinations) may develop in patients with Parkinson's disease, psychosis due to dopaminomimetic therapy is much more common. When such symptoms develop, the accepted first step is to taper anti-parkinsonian medications were possible. Anticholinergic medications, amantadine, selegiline, and dopamine receptor agonists should be reduced or discontinued, provided that the patient can tolerate changes in motor symptoms attendant to such reductions. When these reductions are not feasible or fail to improve treatment-emergent psychosis, low-dose quetiapine or clozapine may be useful. The greatest body of evidence supports the effectiveness of these treatments and their relative lack of adverse effects on motor function. When psychosis develops in the context of epilepsy, the generally accepted first step is to maximize anticonvulsant therapy in an effort to reduce the possible contribution of electrophysiologic disturbances in the described areas to psychotic symptoms. When interictal psychosis persists despite such adjustments, initiation with low-dose atypical antipsychotics carries the least risk of lowering seizure threshold and should be considered.

eldepryl reviews 2017-03-05

Tissue concentrations of MPP+ (1-methyl-4-phenylpyridinium) were measured in buy eldepryl Charles River CFW mice after administration of high doses of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) or MPP+ given subcutaneously or orally, to investigate the relationships between tissue concentrations and lethality resulting from these compounds. MPTP given subcutaneously led to much higher concentrations of MPP+ in brain and somewhat higher concentrations of MPP+ in peripheral tissues than did MPTP given orally. MPTP caused no lethality at oral doses up to 160 mg/kg whereas subcutaneous MPTP had an LD50 of 54 mg/kg. Deprenyl pretreatment antagonized the lethality of subcutaneous MPTP and reduced MPP+ concentrations in brain and in other tissues after MPTP injection. Deprenyl caused a greater and longer-lasting inhibition of MPTP oxidation than of phenylethylamine oxidation, especially in liver, although both compounds are thought to be oxidized by monoamine oxidase type B. The protective effect of deprenyl against MPTP lethality implicates MPP+ (or possibly some other metabolite) in the lethality after MPTP injection. The reduced lethality of MPTP when given orally and the relative lack of brain levels of MPTP or MPP+ after oral MPTP implicate the brain as a target organ in the lethality of MPTP. Lethality after MPP+ administration almost certainly does not involve the brain, since little or no MPP+ could be measured in brain after oral or subcutaneous dosing of MPP+.

eldepryl dosing 2015-08-17

The four treatment buy eldepryl arms were (1) selegiline-placebo and tocopherol-placebo, (2) selegiline-placebo and active tocopherol (2000 IU/d), (3) active selegiline hydrochloride (10 mg/d) and tocopherol-placebo, and (4) active selegiline hydrochloride (10 mg/d) and active tocopherol (2000 IU/d).

eldepryl drug classification 2017-01-01

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) destroys nigrostriatal dopaminergic pathways and thereby produces a syndrome similar to Parkinson's disease. MPTP is oxidized by monoamine oxidase B (MAO B) to the 1-methyl-4-phenylpyridinium ion (MPP+), which is taken up in dopaminergic neurons through the dopamine (DA) uptake system, where it develops its toxic effect. Our observations show a buy eldepryl new aspect of the MPP+ mode of action, in which deprenyl in mice has a partially protective effect against MPP+. Furthermore budipine, a therapeutic agent for Parkinsonism, is also able to partially prevent MPP+ toxicity. A MAO B-inhibitory component of budipine, as shown in receptor binding studies previously, could contribute to this effect. Comparable experiments with nomifensine do not exclude the possibility of budipine as an effect as a DA uptake inhibitor. An unexplained after effect of budipine leads to a large increase in 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) levels five weeks after the last administration.

buy eldepryl online 2017-06-04

The studies included were not identical in design. The studies were registrational in nature and thus not necessarily generalizable. buy eldepryl

eldepryl cost 2015-05-07

HIV-1 infected individuals with impaired cognitive functioning were enrolled in this placebo-controlled, three-arm study of STS across 17 sites. Cognitive impairment was determined using a standard battery of neuropsychological tests. Subjects were randomized to receive STS 3 mg/24 hours, STS 6 mg/24 hours, or matching placebo buy eldepryl patches daily. The primary efficacy endpoint was defined as the change in neuropsychological composite Z-score (NPZ-6) from baseline to week 24. Measures of safety included frequencies of adverse experiences and abnormal results on laboratory tests.

eldepryl medication 2015-09-16

N-isopropyl p-iodoamphetamine (IMP) demonstrates a high affinity for lung and brain during the first pass following intravenous injection. Its high brain affinity has been used to advantage for cerebral perfusion imaging, but the effects of drugs on IMP distribution could affect its utility. In this study, we determined the effects of the tricyclic antidepressant imipramine and the MAO inhibitors deprenyl and phenelzine on the biodistribution of IMP. We first determined the effect of loading dose and anesthesia on the biodistribution of IMP. In rats, biodistribution was not dependent on loading dose between 0.1 and 1.1 mg/kg. Anesthesia with thiopental and chloral hydrate depressed lung and brain IMP uptake. In rats, preloading doses of imipramine depressed lung uptake but did not result in increased brain IMP uptake; postloading doses of imipramine did not release IMP from the lung. In rabbits, simultaneous or postloading doses of imipramine resulted in release of IMP from the lung with an increase in brain activity. Both mixed A and B MAO inhibitors (phenelzine) and B selective MAO inhibitors (deprenyl) did not affect IMP distribution in rats. Based on the action of imipramine on IMP uptake and clearance in the buy eldepryl lung, we postulate that IMP uptake and metabolism within the lung is related to the mixed function oxidase (MFO) system. As the lung is rich in the MFO system in humans, we would also predict from this study that IMP distribution in patients under antidepressant therapy would not be affected by either tricyclic or MAO inhibitor agents apart from the effect of these drugs on cerebral perfusion.

eldepryl tablets 2016-03-03

On the long term Parkinson Disease (PD) treatment is often complicated buy eldepryl by the occurrence of motor fluctuations. To find out whether early treatment of PD with levodopa, dopaminoagonists or l-deprenyl is associated with any difference in motor fluctuations occurrence, the Italian Parkinson Study Group initiated a multicenter, randomized study. Since November 1988, 475 patients requiring effective treatment for idiopathic PD have been randomized to receive levodopa, dopamine agonists or deprenyl. After 2 months of therapy, all patients evaluated with the Unified Parkinson Disease Rating Scale showed a significant amelioration. Daily living activities were more impaired in patients treated with deprenyl. Study design is presented and first results are discussed.

eldepryl dosage forms 2015-12-20

Working independently, we extracted data. For dichotomous data we calculated Protonix 30 Mg random effects odds ratios (OR) with 95% confidence intervals (CI) and, where appropriate, the number needed to treat (NNT) on an intention-to-treat basis. For continuous data we calculated weighted mean differences on the basis of a random effects model. We analysed crossover trials under consideration of correlation of paired measures.

eldepryl drug interactions 2015-08-24

The present study compared the antiimmobility Karela Medicine effects of l-deprenyl (DEP) and moclobemide (MOC) to the classic antidepressant imipramine (IMI), using an ethological approach. To investigate the degree of MAO-B inhibition by DEP and MOC, combination of treatments of ineffective doses of phenylethylamine (PHEA) with DEP or with MOC were administered in three doses before immobility was tested in the forced-swimming paradigm. Tests were videotape recorded for analysis of the frequency and duration of the behaviors during the procedure. There was a significant, dose-dependent decrease in immobility duration and an increase in mobility duration of rats treated with IMI. Both active behaviors of climbing and swimming were equally enhanced by the tricyclic antidepressant, climbing behavior composing 75% of the mobile behaviors. The intermediate doses of the MAOIs tested, DEP 0.25 mg/kg and MOC 30 mg/kg, decreased immobility and increased mobility. The antiimmobility effect of DEP was due to longer climbing behavior while MOC enhanced swimming duration. No behavioral changes were seen with the administration of the lower and higher doses of the MAOI. Potentiation of the antiimmobility effects was observed when ineffective doses of PHEA and of DEP or MOC were administered in combination. Differences between the MAO inhibitors on the active behaviors were also observed when administered with PHEA; DEP and PHEA significantly increased climbing and MOC and PHEA increased swimming. This preclinical evaluation of selective MAO inhibitors indicates that both MAO-A and MAO-B inhibitors have antidepressant effects. However, to clearly demonstrate that these antiimmobility effects are a consequence of increased brain concentrations of any one of the several monoamines implicated in the mechanism of action of DEP or MOC should be the subject of future studies.

eldepryl drug 2017-05-12

These results suggest that (1) development of mammary tumors is mediated through the loss of immunity and sympathetic NA nerve fibers accompanied by reduced NE levels in the Zyrtec Equate Brand spleen, (2) the prevention of mammary tumor development by deprenyl may involve the reversal of the tumor-associated decline in sympathetic NA activity and cell-mediated immune responses in the spleen and DLN and (3) the antitumor effects of deprenyl may be partially mediated through ER-dependent intracellular signaling pathways.

eldepryl and alcohol 2016-08-15

Mechanisms of genetically determined alcoholic motivation were studied in chronically alcohol treated rats and their offspring using neurochemical, physiological and genetic techniques. Stimulation of the activity of membrane-bound monoamine oxidases, (e.g., in liver or brain), modification of their catalytic properties, partial solubilisation and increased sensitivity towards the transitory inhibiting effect of ethanol were detected in chronically alcohol treated rats, especially in offspring which did not receive chronic alcohol treatment. An altered content of biogenic amines in brain and disturbances of behaviour accompanied impairments in functions of monoamine oxidases. Administration of ethanol was required to restore to normal the disturbances in the neurochemical and physiological parameters studied. The constant presence of ethanol in tissues becomes essential for returning metabolic impairments to normal and may be considered as a molecular basis for the development of alcoholic motivation in offspring of chronically alcohol treated animals. A distinct increase in the expression of the c-fos gene in the brain cortex was observed in offspring of chronically alcohol treated rats after administration of ethanol. The impairments in regulating c-fos gene Botox Cost Nj activity caused by ethanol administration suggest that chronic alcohol treatment of animals may influence the functions of the genome of offspring not subjected to chronic alcohol treatment.

eldepryl generic name 2015-10-14

Pharmacy data on members of a large Israeli health maintenance organization, treated as patients with PD during 2001-2012 and prescribed selegiline or rasagiline as their first APD, were analyzed. The first APD was selegiline for 349 patients (2001-2006) and rasagiline for 485 patients (2007-2012). Time from monoamine oxidase type B inhibitor prescription until initiating treatment with dopamine agonists (DAs) or levodopa was compared between the Sustiva Drug groups using Cox regression adjusted to sex and age at initiation of APD.

eldepryl syrup 2015-03-08

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. Paracetamol Syrup 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 < 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 medication dose 2017-11-10

Selegiline is beneficial to Parkinsonian patients as an adjunct to levodopa therapy. A sensitive flourimetric assay based on inhibition of rat brain monoamine oxidase-B (MAO-B) in vitro has been developed to study the pharmacokinetics of selegiline. This method quantitates selegiline as low as 0.25 ng ml-1. The pharmacokinetics and relative bioavailability of selegiline were investigated in healthy volunteers following oral administration of 10 mg tablet or solution. A half-life of approximately 70 min was observed following the administration of either dosage form. Although the two dosage forms exhibited a lag time, the absorption was rapid and peak plasma concentrations were observed between 30 and 45 min for the solution and 30 and 90 min for the tablets. Statistically no significant difference was found between Cmax, Tmax, AUC0-infinity and MRT between the two dosage forms. Negligible renal clearance was found in both groups, but apparent oral plasma clearance was comparatively high and indicates rapid elimination of selegiline from the body.

eldepryl buy 2016-06-13

Effects of a selective monoamine oxidase (MAO)--A inhibitor, clorgyline, a selective MAO-B inhibitor, deprenyl, and a non-selective MAO inhibitor, nialamide, were investigated on footshock-induced aggression (FIA) in paired rats. The doses and pretreatment times of the inhibitors used were based on an earlier reported in vivo dose-response and time-course study. In addition, apomorphine, a dopaminergic receptor agonist, and beta-phenylethylamine, a preferred substrate for MAO-B, were also used to garner corroborative evidence. The results of the study indicate that selective MAO-A inhibitors are likely to attenuate FIA by augmenting central serotonergic activity, while selective MAO-B inhibitors accentuate the behaviour by facilitating dopaminergic activity. A permissive role for noradrenaline could not be delineated by the available data.

eldepryl order 2016-08-21

After acute administration of the monoamine oxidase inhibitor clorgyline there is a reduction of aromatic L-amino acid decarboxylase and tyrosine hydroxylase activity in the mouse striatum. Similar responses were seen after administering the non-selective monoamine oxidase inhibitor pargyline and high, but not low, doses of the selective monoamine oxidase-B inhibitor deprenyl. Changes of tyrosine hydroxylase activity were observed only when subsaturated concentrations of the pteridine cofactor were used for the assay. The monoamine oxidase inhibitors altered the abundance of aromatic L-amino acid decarboxylase and tyrosine hydroxylase mRNA in the midbrain. Pargyline and high doses of deprenyl increased, aromatic L-amino acid decarboxylase mRNA, while clorgyline initially decreased and then increased it. All three compounds caused an early decrease of tyrosine hydroxylase mRNA. The acidic metabolites of dopamine appeared most affected by pargyline and clorgyline, supporting the notion that deamination of striatal dopamine in rodents is primarily by monoamine oxidase-A. Our results suggest, that striatal tyrosine hydroxylase and aromatic L-amino acid decarboxylase are apparently modulated via different mechanisms in response to perturbation of dopamine metabolism.

eldepryl generic 2017-10-19

Cell therapy is one of the approaches taken to treatment of spinal cord disorders. In this study, adipose-derived stem cells (ADSCs) were induced to form motoneuron-like cells (MNLCs) using selegiline as preinducer, as well as Shh and all trans-retinoic acid (RA) as inducers. Selegiline was reported to induce the embryonic stem cells and bone marrow stromal cells into neuronal phenotype. ADSCs were evaluated using CD90, CD44, CD 49d, CD106, CD31, CD45, lipogenesis and osteogenesis. Dose response and time course studies were used in selecting the optimal concentration for selegiline using the percentage of viable cells (PVC) and percentages of immunoreactive cells (PIC) to nestin and neurofilament 68. Accordingly, such studies were used in selecting the optimal dose for RA using PVC and PIC to islet-1 and oligo-2. The expression of islet-1, oligo-2 and HLXB9 was evaluated using RT-PCR and immunocytochemistry. Real-time PCR was utilized in order to quantify the expression of islet-1, oligo-2 and HLXB9. ADSCs were immunoreactive to CD90, CD44 and CD 49d with consistent differentiation osteogenic and lipogenic cells. The optimal concentrations of selegiline and RA were 10⁻⁹ mM and 2 × 10⁻⁸ M, respectively. After two days, MNLCs showed high oligo-2 expression. MNLCs innervated myotubes; also, the release rate of synaptic vesicles using FM1-43 followed exponential decay model, and this rate in the induced MNLCs was approximately three times of that in the preinduced cells.

cost of eldepryl 2017-08-02

Results indicated that female dog and male Micropig skin were reasonable animal models for 24 hour in vitro selegiline penetration through human skin. Penetration of selegiline through rat skin and hairless mouse skin was 2-fold and 3-fold higher than through human skin, respectively. Metabolism was negligible in human skin. Selegiline metabolites (L-methamphetamine and N-desmethylselegiline but not L-amphetamine) were detected at all time points but the extent of selegiline metabolism was negligible. The cumulative 24 hour in vitro selegiline permeation from a 1.83 mg/cm2 STS through human skin was 5.0 mg. This was similar to the in vivo permeation in humans as assessed by residual patch analysis.

eldepryl 5 mg 2017-01-17

Parkinson's disease generally responds well to dopaminergic therapy, but there is no unanimity concerning the optimal time for introducing dopaminergic medication. Dose-related side effects of these drugs may respond to a drug holiday, and fluctuations in response to levodopa may sometimes be helped by addition of bromocriptine to the drug regimen. Anticholinergic drugs, tricyclic compounds, and amantadine may sometimes lead to benefit, but any antiparkinsonian effect is often disappointing. Mental side effects may occur with all of the antiparkinsonian drugs, particularly the anticholinergic agents, and especially in the elderly.