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Selegiline on Pubmed
Neurol Res. 2002 Mar;24(2):169-73.
Inhibition of human LDL oxidation by the neuroprotective drug l-deprenyl.
Thomas T, Bhavnani BR, Thomas P.
Woodlands Medical Center, 3150 Tampa Road, Oldsmar, Florida 34677, USA. [email protected]
L-deprenyl (Selegiline) used in the treatment of Parkinson's and Alzheimer's disease also enhances longevity. Oxidized low density lipoprotein promotes atherosclerosis and is toxic to both vascular and neural tissue. The reported association between vascular dysfunction and neurodegenerative diseases prompted us to investigate the effect of l-deprenyl, a MAO-B inhibitor, on low density lipoprotein (LDL) oxidation. LDL was isolated from freshly collected blood and the kinetics of copper induced oxidation of LDL was monitored continuously by spectrophotometry. Oral administration (10 mg) or in vitro (2.8 to 84 microM) addition of l-deprenyl inhibited oxidation of LDL isolated from healthy men and post-menopausal women. This is the first report demonstrating that the antioxidant action of l-deprenyl may be antiatherogenic and cardioprotective. Such an action could contribute to reported extension of life span associated with long-term administration of the drug. In conjunction with inhibition of LDL oxidation, l-deprenyl is unique in that it demonstrates protective effects on both vascular and neuronal tissue. Prophylactic use of low doses of l-deprenyl may accord protection against vascular and neurodegenerative diseases associated with aging.
Life Sci. 2000 Jan 21;66(9)
L141-6.
Evidence that gingko biloba extract does not inhibit MAO A and B in living human brain.
Fowler JS, Wang GJ, Volkow ND, Logan J, Franceschi D, Franceschi M, MacGregor R, Shea C, Garza V, Liu N, Ding YS.
Department of Chemistry, Brookhaven National Laboratory, Upton, NY 11973-5000, USA. [email protected]
Extracts of Ginkgo biloba have been reported to reversibly inhibit both monoamine oxidase (MAO) A and B in rat brain in vitro leading to speculation that MAO inhibition may contribute to some of its central nervous system effects. Here we have used positron emission tomography (PET) to measure the effects of Ginkgo biloba on human brain MAO A and B in 10 subjects treated for 1 month with 120 mg/day of the Ginkgo biloba extract EGb 761, using [11C]clorgyline and [11C]L-deprenyl-D2 to measure MAO A and B respectively. A three-compartment model was used to calculate the plasma to brain transfer constant K1 which is related to blood flow, and lambdak3, a model term which is a function of the concentration of catalytically active MAO molecules. Ginkgo biloba administration did not produce significant changes in brain MAO A or MAO B suggesting that mechanisms other than MAO inhibition need to be considered as mediating some of its CNS effects.
J Neural Transm Suppl. 1998;52:321-8.
Selegiline as immunostimulant--a novel mechanism of action?
Müller T, Kuhn W, Krüger R, Przuntek H.
Department of Neurology, St. Josef-Hospital, University of Bochum, Federal Republic of Germany.
In clinical studies the MAO-B inhibitor selegiline appears to slow the progression of neurological deficits in Parkinson's disease (PD) and the cognitive decline in Alzheimer's disease (AD). The mechanisms of action remain unclear. Several lines of evidence indicate an immune-mediated pathophysiology of PD and AD. According to animal trials, selegiline increases the survival rate of immune suppressed mice. Stimulation of the immune response to bacterial or viral infection or in chronic inflammatory processes in managed by an increased synthesis of the cytokines interleukin-1 beta (IL-1 beta) and subsequent interleukin-6 (IL-6). Outcome of viral or bacterial infections in the brain highly correlates with levels of the cytotoxic cytokine tumor-necrosis-factor-alpha (TNF). The aim of our study was to characterize the influence of selegiline on the biosynthesis of IL-1 beta, IL-6 and TNF in human peripheral blood mononuclear cells (PBMC) from healthy blood donors. After isolation and washing PBMC were cultured without and with selegiline in three different concentrations (0.01 mumol/l, 0.001 mumol/l, 0.0001 mumol/l) in a humidified atmosphere (7% CO2). Then cultures were centrifuged and supernatants were collected for IL-1 beta, IL-6 and TNF ELISA-assays. Treatment of cultured PBMC with various concentrations induced an increased synthesis of IL-1 beta (ANOVA F = 9.703, p = 0.0007), IL-6 (ANOVA F = 20.648, p = 0.0001) and a reduced production of TNF (ANOVA F = 3.770, p = 0.040). These results indicate, that the influence of selegiline on the cytokine biosynthesis may also contribute to its putative neuroprotective properties.
J Neuropsychiatry Clin Neurosci. 1996 Spring;8(2):168-71.
Sustained antidepressant effect of PEA replacement.
Sabelli H, Fink P, Fawcett J, Tom C.
Rush University and the Center for Creative Development, Chicago, Illinois, USA.
Phenylethylamine (PEA), an endogenous neuroamine, increases attention and activity in animals and has been shown to relieve depression in 60% of depressed patients. It has been proposed that PEA deficit may be the cause of a common form of depressive illness. Fourteen patients with major depressive episodes that responded to PEA treatment (10-60 mg orally per day, with 10 mg/day selegiline to prevent rapid PEA destruction) were reexamined 20 to 50 weeks later. The antidepressant response had been maintained in 12 patients. Effective dosage did not change with time. There were no apparent side effects. PEA produces sustained relief of depression in a significant number of patients, including some unresponsive to the standard treatments. PEA improves mood as rapidly as amphetamine but does not produce tolerance.
J Neural Transm Suppl. 1995;45:271-9.
Interaction of neuroprotective substances with human brain superoxide dismutase. An in vitro study.
Gsell W, Reichert N, Youdim MB, Riederer P.
Department of Psychiatry, Clinical Neurochemistry, University of Würzburg, Federal Republic of Germany.
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.
Arch Gen Psychiatry. 1989 Jan;46(1):45-50.
A controlled study of the antidepressant efficacy and side effects of (-)-deprenyl. A selective monoamine oxidase inhibitor.
Mann JJ, Aarons SF, Wilner PJ, Keilp JG, Sweeney JA, Pearlstein T, Frances AJ, Kocsis JH, Brown RP.
Department of Psychiatry, Cornell University Medical College, New York, NY 10021.
Monoamine oxidase (MAO) inhibitors are effective antidepressants whose use is limited because of unwanted side effects and the possibility of a tyramine-induced hypertensive crisis (cheese reaction). (-)-Deprenyl (the official nonproprietary name for this substance is selegiline), a selective MAO type B inhibitor, may be safer and have fewer side effects, but its antidepressant efficacy is uncertain. A double-blind placebo-controlled study was carried out in depressed outpatients who were treated with (-)-deprenyl in an MAO type B selective dose range and at a higher nonselective dose range. (-)-Deprenyl did not have a statistically significant antidepressant effect after three weeks of treatment at doses of 10 mg/d. However, after six weeks and at higher doses (averaging about 30 mg/d for the second three weeks), (-)-deprenyl was superior to placebo in antidepressant effect with a positive response rate of 50% vs 13.6% and with a 41% reduction in the Hamilton Depression Rating Scale mean score vs 10% in the placebo-treated group. No hypertensive crises were seen. The rate of occurrence of side effects with (-)-deprenyl was no greater than with placebo. It was concluded that (-)-deprenyl is an effective antidepressant in a dose range where it is distinguished by the absence of many of the side effects typical of nonselective MAO inhibitors.
J Clin Psychiatry. 1986 Nov;47(11):563-5.
Mysterious MAOI hypertensive episodes.
Linet LS.
A reliable patient experienced several MAOI-associated acute hypertensive episodes that could not be accounted for by indiscretions of diet or contraindicated medications. The sparse literature on such mysterious hypertensive crises reveals them to be uncommon but not unknown. The mechanism is as yet disturbingly unexplained. An incidental finding in this case was that the novel MAOI l-deprenyl did not result in hypertensive crises but, in contrast to conventional MAOIs, was ineffective against panic attacks.
Neurology. 1982 May;32(5):503-9.
Metabolism of (-) deprenyl to amphetamine and methamphetamine may be responsible for deprenyl's therapeutic benefit: a biochemical assessment.
Karoum F, Chuang LW, Eisler T, Calne DB, Liebowitz MR, Quitkin FM, Klein DF, Wyatt RJ.
The urinary excretion of some important phenylethylamines, catecholamines, their metabolites, amphetamine, and methamphetamine were measured in parkinsonian patients on Sinemet (L-dopa plus carbidopa, a peripheral dopadecarboxylase inhibitor) and depressed patients after chronic (-) deprenyl treatment. Deprenyl was efficiently metabolized to amphetamine and methamphetamine. It increased the excretion of phenylethylamine and of m- and p-tyramine, and reduced the output of norepinephrine metabolites, but failed to alter the excretion of dopamine-deaminated metabolites. These changes were attributed more to amphetamine and methamphetamine than to inhibition of monoamine oxidase type B. Sinemet treatment alone increased the excretion of dopamine, 3-methoxytyramine, and their respective deaminated metabolites, 3, 4-dihydroxyphenylacetic acid and homovanillic acid. It is concluded that conversion of deprenyl to amphetamine and methamphetamine may contribute to some of the therapeutic benefits of deprenyl.
J Neural Transm. 1981;51(3-4):223-31.
Effects of L-deprenyl on human growth hormone secretion.
Koulu M, Lammintausta R.
The effects of L-deprenyl on L-dopa-, apomorphine- and L-tryptophan-induced growth hormone (GH) secretion were studied in thirteen healthy male volunteers. An acute 10 mg dose of L-deprenyl did not stimulate the basal GH secretion. Short-term L-deprenyl premedication significantly enhanced the L-dopa-stimulated GH release. In contrast, L-deprenyl premedication did not change the GH response to apomorphine or L-tryptophan. Potentiation of L-dopa-induced GH release by L-deprenyl indicates an increased availability of dopamine at the receptor level without a direct agonistic effect by the drug. Furthermore, L-deprenyl does not change the function of postsynaptic dopamine receptors involved in human GH release.
Psychopharmacology (Berl). 1980;70(2):163-6.
The effect of deprenyl, a selective monoamine oxidase B inhibitor, on sleep and mood in man.
Thornton C, Doré CJ, Elsworth JD, Herbert M, Stern GM.
The effect of (-)-deprenyl, a rapidly acting selective monoamine oxidase (MAO) B inhibitor, on the sleep and mood of six healthy young male adults was investigated. The drug was administered double-blind in a balanced cross-over design. The dose (5-10 mg/day for 3 days) was chosen to cause complete inhibition of MAO, a process which usually takes 1-2 weeks with conventional MAO inhibitors. The inhibition was monitored by measuring platelet MAO activity and phenylethylamine excretion. Urinary phenylethylamine concentration was raised in all subjects. Subjects were unaware of any sleep disturbance due to the drug although the electroencephalogram (EEG) showed increased wakefulness. The onset of rapid-eye-movement (REM) sleep was delayed and the total amount reduced; the amount of stage 2 sleep was increased. The only effect of the drug on mood was to decrease the level of alertness prior to sleep. There was a slight but significant increase in the pre-sleep systolic blood pressure. There were no effects due to drug withdrawal.
J Affect Disord. 1980 Jun;2(2):137-46.
Antidepressant potentiation of 5-hydroxytryptophan by L-deprenil in affective illness.
Mendlewicz J, Youdim MB.
In an open trial study, L-Deprenil, an irreversible selective MAO-B inhibitor without 'chesse effect' was given to 14 patients with unipolar and bipolar depression receiving L-5-Hydroxytryptophan (L-5-HTP) and benzerazide. Ten out of 14 patients showed a good response to the combination of drugs and a correlation was found between the degree of platelet MAO inhibition and clinical response. In a double-blind controlled study, 18 affectively ill patients were randomly allocated to L-Deprenil plus L-5-HTP and benzerazide, 21 patients were treated with L-5-HTP and benzerazide and 19 patients with placebo only. Patients treated with the combination of L-Deprenil and L-5-HTP showed a significantly greater clinical improvement than placebo patients but this was not the case for patients treated with 5-HTP alone. A positive relationship was demonstrated between mood improvement and degree of platelet MAO inhibition in patients treated with L-Deprenil.
Neurol Res. 2002 Mar;24(2):169-73.
Inhibition of human LDL oxidation by the neuroprotective drug l-deprenyl.
Thomas T, Bhavnani BR, Thomas P.
Woodlands Medical Center, 3150 Tampa Road, Oldsmar, Florida 34677, USA. [email protected]
L-deprenyl (Selegiline) used in the treatment of Parkinson's and Alzheimer's disease also enhances longevity. Oxidized low density lipoprotein promotes atherosclerosis and is toxic to both vascular and neural tissue. The reported association between vascular dysfunction and neurodegenerative diseases prompted us to investigate the effect of l-deprenyl, a MAO-B inhibitor, on low density lipoprotein (LDL) oxidation. LDL was isolated from freshly collected blood and the kinetics of copper induced oxidation of LDL was monitored continuously by spectrophotometry. Oral administration (10 mg) or in vitro (2.8 to 84 microM) addition of l-deprenyl inhibited oxidation of LDL isolated from healthy men and post-menopausal women. This is the first report demonstrating that the antioxidant action of l-deprenyl may be antiatherogenic and cardioprotective. Such an action could contribute to reported extension of life span associated with long-term administration of the drug. In conjunction with inhibition of LDL oxidation, l-deprenyl is unique in that it demonstrates protective effects on both vascular and neuronal tissue. Prophylactic use of low doses of l-deprenyl may accord protection against vascular and neurodegenerative diseases associated with aging.
Life Sci. 2000 Jan 21;66(9)
L141-6.Evidence that gingko biloba extract does not inhibit MAO A and B in living human brain.
Fowler JS, Wang GJ, Volkow ND, Logan J, Franceschi D, Franceschi M, MacGregor R, Shea C, Garza V, Liu N, Ding YS.
Department of Chemistry, Brookhaven National Laboratory, Upton, NY 11973-5000, USA. [email protected]
Extracts of Ginkgo biloba have been reported to reversibly inhibit both monoamine oxidase (MAO) A and B in rat brain in vitro leading to speculation that MAO inhibition may contribute to some of its central nervous system effects. Here we have used positron emission tomography (PET) to measure the effects of Ginkgo biloba on human brain MAO A and B in 10 subjects treated for 1 month with 120 mg/day of the Ginkgo biloba extract EGb 761, using [11C]clorgyline and [11C]L-deprenyl-D2 to measure MAO A and B respectively. A three-compartment model was used to calculate the plasma to brain transfer constant K1 which is related to blood flow, and lambdak3, a model term which is a function of the concentration of catalytically active MAO molecules. Ginkgo biloba administration did not produce significant changes in brain MAO A or MAO B suggesting that mechanisms other than MAO inhibition need to be considered as mediating some of its CNS effects.
J Neural Transm Suppl. 1998;52:321-8.
Selegiline as immunostimulant--a novel mechanism of action?
Müller T, Kuhn W, Krüger R, Przuntek H.
Department of Neurology, St. Josef-Hospital, University of Bochum, Federal Republic of Germany.
In clinical studies the MAO-B inhibitor selegiline appears to slow the progression of neurological deficits in Parkinson's disease (PD) and the cognitive decline in Alzheimer's disease (AD). The mechanisms of action remain unclear. Several lines of evidence indicate an immune-mediated pathophysiology of PD and AD. According to animal trials, selegiline increases the survival rate of immune suppressed mice. Stimulation of the immune response to bacterial or viral infection or in chronic inflammatory processes in managed by an increased synthesis of the cytokines interleukin-1 beta (IL-1 beta) and subsequent interleukin-6 (IL-6). Outcome of viral or bacterial infections in the brain highly correlates with levels of the cytotoxic cytokine tumor-necrosis-factor-alpha (TNF). The aim of our study was to characterize the influence of selegiline on the biosynthesis of IL-1 beta, IL-6 and TNF in human peripheral blood mononuclear cells (PBMC) from healthy blood donors. After isolation and washing PBMC were cultured without and with selegiline in three different concentrations (0.01 mumol/l, 0.001 mumol/l, 0.0001 mumol/l) in a humidified atmosphere (7% CO2). Then cultures were centrifuged and supernatants were collected for IL-1 beta, IL-6 and TNF ELISA-assays. Treatment of cultured PBMC with various concentrations induced an increased synthesis of IL-1 beta (ANOVA F = 9.703, p = 0.0007), IL-6 (ANOVA F = 20.648, p = 0.0001) and a reduced production of TNF (ANOVA F = 3.770, p = 0.040). These results indicate, that the influence of selegiline on the cytokine biosynthesis may also contribute to its putative neuroprotective properties.
J Neuropsychiatry Clin Neurosci. 1996 Spring;8(2):168-71.
Sustained antidepressant effect of PEA replacement.
Sabelli H, Fink P, Fawcett J, Tom C.
Rush University and the Center for Creative Development, Chicago, Illinois, USA.
Phenylethylamine (PEA), an endogenous neuroamine, increases attention and activity in animals and has been shown to relieve depression in 60% of depressed patients. It has been proposed that PEA deficit may be the cause of a common form of depressive illness. Fourteen patients with major depressive episodes that responded to PEA treatment (10-60 mg orally per day, with 10 mg/day selegiline to prevent rapid PEA destruction) were reexamined 20 to 50 weeks later. The antidepressant response had been maintained in 12 patients. Effective dosage did not change with time. There were no apparent side effects. PEA produces sustained relief of depression in a significant number of patients, including some unresponsive to the standard treatments. PEA improves mood as rapidly as amphetamine but does not produce tolerance.
J Neural Transm Suppl. 1995;45:271-9.
Interaction of neuroprotective substances with human brain superoxide dismutase. An in vitro study.
Gsell W, Reichert N, Youdim MB, Riederer P.
Department of Psychiatry, Clinical Neurochemistry, University of Würzburg, Federal Republic of Germany.
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.
Arch Gen Psychiatry. 1989 Jan;46(1):45-50.
A controlled study of the antidepressant efficacy and side effects of (-)-deprenyl. A selective monoamine oxidase inhibitor.
Mann JJ, Aarons SF, Wilner PJ, Keilp JG, Sweeney JA, Pearlstein T, Frances AJ, Kocsis JH, Brown RP.
Department of Psychiatry, Cornell University Medical College, New York, NY 10021.
Monoamine oxidase (MAO) inhibitors are effective antidepressants whose use is limited because of unwanted side effects and the possibility of a tyramine-induced hypertensive crisis (cheese reaction). (-)-Deprenyl (the official nonproprietary name for this substance is selegiline), a selective MAO type B inhibitor, may be safer and have fewer side effects, but its antidepressant efficacy is uncertain. A double-blind placebo-controlled study was carried out in depressed outpatients who were treated with (-)-deprenyl in an MAO type B selective dose range and at a higher nonselective dose range. (-)-Deprenyl did not have a statistically significant antidepressant effect after three weeks of treatment at doses of 10 mg/d. However, after six weeks and at higher doses (averaging about 30 mg/d for the second three weeks), (-)-deprenyl was superior to placebo in antidepressant effect with a positive response rate of 50% vs 13.6% and with a 41% reduction in the Hamilton Depression Rating Scale mean score vs 10% in the placebo-treated group. No hypertensive crises were seen. The rate of occurrence of side effects with (-)-deprenyl was no greater than with placebo. It was concluded that (-)-deprenyl is an effective antidepressant in a dose range where it is distinguished by the absence of many of the side effects typical of nonselective MAO inhibitors.
J Clin Psychiatry. 1986 Nov;47(11):563-5.
Mysterious MAOI hypertensive episodes.
Linet LS.
A reliable patient experienced several MAOI-associated acute hypertensive episodes that could not be accounted for by indiscretions of diet or contraindicated medications. The sparse literature on such mysterious hypertensive crises reveals them to be uncommon but not unknown. The mechanism is as yet disturbingly unexplained. An incidental finding in this case was that the novel MAOI l-deprenyl did not result in hypertensive crises but, in contrast to conventional MAOIs, was ineffective against panic attacks.
Neurology. 1982 May;32(5):503-9.
Metabolism of (-) deprenyl to amphetamine and methamphetamine may be responsible for deprenyl's therapeutic benefit: a biochemical assessment.
Karoum F, Chuang LW, Eisler T, Calne DB, Liebowitz MR, Quitkin FM, Klein DF, Wyatt RJ.
The urinary excretion of some important phenylethylamines, catecholamines, their metabolites, amphetamine, and methamphetamine were measured in parkinsonian patients on Sinemet (L-dopa plus carbidopa, a peripheral dopadecarboxylase inhibitor) and depressed patients after chronic (-) deprenyl treatment. Deprenyl was efficiently metabolized to amphetamine and methamphetamine. It increased the excretion of phenylethylamine and of m- and p-tyramine, and reduced the output of norepinephrine metabolites, but failed to alter the excretion of dopamine-deaminated metabolites. These changes were attributed more to amphetamine and methamphetamine than to inhibition of monoamine oxidase type B. Sinemet treatment alone increased the excretion of dopamine, 3-methoxytyramine, and their respective deaminated metabolites, 3, 4-dihydroxyphenylacetic acid and homovanillic acid. It is concluded that conversion of deprenyl to amphetamine and methamphetamine may contribute to some of the therapeutic benefits of deprenyl.
J Neural Transm. 1981;51(3-4):223-31.
Effects of L-deprenyl on human growth hormone secretion.
Koulu M, Lammintausta R.
The effects of L-deprenyl on L-dopa-, apomorphine- and L-tryptophan-induced growth hormone (GH) secretion were studied in thirteen healthy male volunteers. An acute 10 mg dose of L-deprenyl did not stimulate the basal GH secretion. Short-term L-deprenyl premedication significantly enhanced the L-dopa-stimulated GH release. In contrast, L-deprenyl premedication did not change the GH response to apomorphine or L-tryptophan. Potentiation of L-dopa-induced GH release by L-deprenyl indicates an increased availability of dopamine at the receptor level without a direct agonistic effect by the drug. Furthermore, L-deprenyl does not change the function of postsynaptic dopamine receptors involved in human GH release.
Psychopharmacology (Berl). 1980;70(2):163-6.
The effect of deprenyl, a selective monoamine oxidase B inhibitor, on sleep and mood in man.
Thornton C, Doré CJ, Elsworth JD, Herbert M, Stern GM.
The effect of (-)-deprenyl, a rapidly acting selective monoamine oxidase (MAO) B inhibitor, on the sleep and mood of six healthy young male adults was investigated. The drug was administered double-blind in a balanced cross-over design. The dose (5-10 mg/day for 3 days) was chosen to cause complete inhibition of MAO, a process which usually takes 1-2 weeks with conventional MAO inhibitors. The inhibition was monitored by measuring platelet MAO activity and phenylethylamine excretion. Urinary phenylethylamine concentration was raised in all subjects. Subjects were unaware of any sleep disturbance due to the drug although the electroencephalogram (EEG) showed increased wakefulness. The onset of rapid-eye-movement (REM) sleep was delayed and the total amount reduced; the amount of stage 2 sleep was increased. The only effect of the drug on mood was to decrease the level of alertness prior to sleep. There was a slight but significant increase in the pre-sleep systolic blood pressure. There were no effects due to drug withdrawal.
J Affect Disord. 1980 Jun;2(2):137-46.
Antidepressant potentiation of 5-hydroxytryptophan by L-deprenil in affective illness.
Mendlewicz J, Youdim MB.
In an open trial study, L-Deprenil, an irreversible selective MAO-B inhibitor without 'chesse effect' was given to 14 patients with unipolar and bipolar depression receiving L-5-Hydroxytryptophan (L-5-HTP) and benzerazide. Ten out of 14 patients showed a good response to the combination of drugs and a correlation was found between the degree of platelet MAO inhibition and clinical response. In a double-blind controlled study, 18 affectively ill patients were randomly allocated to L-Deprenil plus L-5-HTP and benzerazide, 21 patients were treated with L-5-HTP and benzerazide and 19 patients with placebo only. Patients treated with the combination of L-Deprenil and L-5-HTP showed a significantly greater clinical improvement than placebo patients but this was not the case for patients treated with 5-HTP alone. A positive relationship was demonstrated between mood improvement and degree of platelet MAO inhibition in patients treated with L-Deprenil.
