Role of B-Type Monoamine Oxidase Inhibition in the Treatment of Parkinson’s Disease

An Update
  • Joseph Knoll


Parkinson’s disease (PD), first described in 1817 as paralysis agitans by James Parkinson in his “Essay on the Shaking Pulsy,” is characterized by tremor, bradykinesia, rigidity, and a postural defect. The usual distinction between postencephalitic and idiopathic PD is of little practical importance as about 85–90% of the patients suffer from the idiopathic form of the illness.


Monoamine Oxidase Decarboxylase Inhibitor Striatal Slice Nigrostriatal Dopaminergic Neuron Peripheral Decarboxylase Inhibitor 
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  1. Ayd, F. J. and Blackwell, B. (eds.), 1970, Discoveries in Biological Psychiatry, J. B. Lippincott, Philadelphia.Google Scholar
  2. Barbeau, A., 1969, L-Dopa therapy in Parkinson’s disease: A critical review of nine years experience, Can. Med. Assoc. J. 101: 791.Google Scholar
  3. Barbeau, A., 1980, High level therapy in severely akinetic parkinsonian patients: twelve years later, in: Parkinson’s Disease. Current Progress, Problems and Management ( U.K. Rinne, M. Klinger, and G. Stamm, eds.) pp. 229–239, Elsevier/North Holland Biomedical Press, Amsterdam, New York.Google Scholar
  4. Barbeau, A., Murphy, C. F., and Sourkes, T. L., 1961, Excretion of dopamine in diseases of basal glanglia, Science 133: 1706.PubMedCrossRefGoogle Scholar
  5. Bartholini, G., Burkhard, W. P., Pletscher, A., and Bates, V. M., 1967, Increase of cerebral catecholamines by L-DOPA after inhibition of peripheral decarboxylase, Nature (London.) 215: 852.CrossRefGoogle Scholar
  6. Bertler, A., and Rosengren, E., 1959, On the distribution in brain monoamines and of enzymes responsible for their formation, Experientia 15: 10.PubMedCrossRefGoogle Scholar
  7. Birkmayer, W., 1969, Experimentelle Ergebnisse Uber die Kombinationsbehandlung des Parkinson-Syndromes mit L-Dopa und einem Decarboxylasehemmer (Ro 4–4602), Wien. klin. Wschr. 81: 677.PubMedGoogle Scholar
  8. Birkmayer, W., 1983, Deprenyl (selegiline) in the treatment of Parkinson’s disease, Acta Neurol. Scand. 95 (Suppl.): 103.CrossRefGoogle Scholar
  9. Birkmayer, W., and Hornykiewicz, O., 1961, Der L-Dioxyphenylalanin (L-DOPA)-effect bei der Parkinson-Akinesia, Wien. klin. Wschr. 73: 787.PubMedGoogle Scholar
  10. Birkmayer, W., and Hornykiewicz, O., 1962, Der-L-dioxyphenylalanin-Effect beim Parkinson-Syndrom des Menschen, Arch. Psychiatr. Nervenkr. 2P3: 560.Google Scholar
  11. Birkmayer, W., and Mentasti, M., 1967, Weitere experimentelle Unterschungen uber des Katecholaminstoffwechsel bei extrapyramidalen Erkrankugen (Parkinson-und Choreasyndrom). Arch. Psych. Z. ges. Neurol. 210:29.CrossRefGoogle Scholar
  12. Birkmayer, W., and Riederer, P.,1983, Parkinson’s Disease Biochemistry, Clinical Pathology and Treatment,Springer-Verlag, Wien, New York.Google Scholar
  13. Birkmayer, W., Riederer, P., Youdim, M. B. H., and Linauer, W., 1975, The potentiation of the anti-akinetic effect after L-DOPA treatment by an inhibitor of MAO-B, Deprenyl, J. Neural. Transm., 36: 303.PubMedCrossRefGoogle Scholar
  14. Birkmayer, W., Riederer, P., Ambrozi, L., and Youdim, M. B. H., 1977, Implications of combined treatment with “Madopar” and L-Deprenyl in Parkinson’s disease, Lancet (I) 8009: 439.Google Scholar
  15. Birkmayer, W., Knoll, J., Riederer, P. and Youdim, M. B. H., 1983, (–)Deprenyl leads to prolongation of L-dopa efficacy in Parkinson’s disease, Mod. Probl. Pharmacopsychiatr. 19: 170.Google Scholar
  16. Blackwell, B., 1963, Hypertensive crisis due to monoamine oxidase inhibitors, Lancet I: 849.CrossRefGoogle Scholar
  17. Blackwell, B., Marley, E., Price, J. and Taylor, D., 1967, Hypertensive interactions between monoamine oxidase inhibitors and foodstuffs, Br. J. Psychiatry. 113: 349.PubMedCrossRefGoogle Scholar
  18. Braestrup, C., Andersen, H., and Randrup, A., 1975, The monoamine oxidase B inhibitor deprenyl potentiates phenylethylamine behavior in rats without inhibition of catecholamine metabolite formation, Eur. J. Pharmacol. 34: 181.PubMedCrossRefGoogle Scholar
  19. Burns, R. S., Chiueh, C. C., Markey, S. P., Ebert, M. H., Jacobowitz, D. M., and Kopin, I. J., 1983, A primate model of parkinsonism: Selective destructions in the pars compacta of the substantia nigra by N-methyl-4–phenyl-1,2,3,6–tetrahydropyridine, Proc. Natl. Acad. Sci. USA 80: 4546.PubMedCrossRefGoogle Scholar
  20. Burns, R. S., Markey, S. P., Phillips, J. M., and Chieuh, C. C., 1984, The neurotoxicity of 1methyl-4–phenyl-1,2,3,6–tetrahydropyridine in the monkey and man, Can. J. Neurol. Sci. 11: 166.PubMedGoogle Scholar
  21. Carlsson, A., 1959, The occurrence distribution and physiological role of catecholamines in the nervous system, Pharmacol. Rev. 11: 490.PubMedGoogle Scholar
  22. Carlsson, A., 1975, Receptor mediated control of dopamine metabolism, in: Pre-and Postsynaptic Receptors ( E. Usdin and W. E. Bunney, eds.), p. 49, Marcel Dekker, New York.Google Scholar
  23. Carlsson, A., and Waldeck, B., 1958, A fluorimetric method for the determination of DA (3–hy-droxytyramine), Acta Physiol. Scand. 44: 293.PubMedCrossRefGoogle Scholar
  24. Chiba, K., Trevor, A., and Castagnoli, N., Jr., 1984, Metabolism of the neurotoxic tertiary amine MPTP, by brain monoamine oxidase, Biochem. Biophys. Res. Commun. 120:574.PubMedCrossRefGoogle Scholar
  25. Chieuh, C. C., Burns, R. S., Markey, S., Jakobowitz, D., Ebert, M. H., and Kopin, I. J., 1983 Effects of N-methyl-4–phenyl-1,2,3,6–tetrahydropyridine, a cause of an extrapyramidal syndrome, on the nigrostriatal dopaminergic system in the rat, guinea pig, and monkey. 5th Catecholamine Symposium, Gothenburg (Abstr.), 74.Google Scholar
  26. Cohen, G., Pasik, P., Cohen, B., Leist, A., Mytilineou, C., and Yahr, M. D. 1985, Pargyline and deprenyl prevent the neurotoxicity of 1–methyl-4–phenyl-1,2,3,6–tetrahydropyridine (MPTP) in monkeys, Eur. J. Pharmacol. 106: 209.CrossRefGoogle Scholar
  27. Cotzias, G. C., Papvasiliov, P. S., and Gellene, R., 1969, Modification of parkinsonism—Chronic treatment with L-dopa, N. Engl. J. Med. 280: 337.PubMedCrossRefGoogle Scholar
  28. Csanda, E., and Tarczy, M., 1983, Clinical evaluation of deprenyl (selegiline) in the treatment of Parkinson’s disease, Acta Neurol. Scand. 95 (Suppl.): 117.CrossRefGoogle Scholar
  29. Csanda, E., Antal, J., Anthony, M., and Csanaky, A., 1978, Experiences with L-deprenyl in parkinsonism, J. Neural. Transm. 43: 263.PubMedCrossRefGoogle Scholar
  30. Csanda, E., Antal, J., and Fornadi, F., 1980, Clinical experience in extrapyramidal disease with selective MAO-B inhibitor, deprenyl, in: Monoamine Oxidases and Their Selective Inhibition ( K. Magyar, ed.), pp. 127–132, Pergamon Press-Akademiai Kiado, Budapest.Google Scholar
  31. Davis, G. C., Williams, A. C., Markey, S. P., Ebert, M. H., Caine, E. D., Reichart, C. M., and Kopin, I. J., 1979, Chronic parkinsonism secondary to intravenous injection of meperidine analogues, Psychiatr. Res. 1: 249.CrossRefGoogle Scholar
  32. Dupont, E., 1977, Epidemiology of Parkinsonism, in: Symposium on Parkinsonism ( J. Worm-Petersen and J. Bottcher, eds.), pp. 65–75, M. S. D., Denmark.Google Scholar
  33. Ehringer, H., and Hornykiewicz, O., 1960, Verteilung von Noradrenalin und Dopamin (3–Hy-droxytyramin) im Gehirn des Menschen und ihr Verhalten bei Erkrankungen des extrapyramidalen Systems, Klin. Wschr. 38: 1336.CrossRefGoogle Scholar
  34. Ekstedt, B., Magyar, K., and Knoll, J., 1979, Does the B form selective monoamine oxidase inhibitor lose selectivity by long term treatment? Biochem. Pharmacol. 28: 919.PubMedCrossRefGoogle Scholar
  35. Elsworth, J. D., Glover, V., Reynolds, G. P., Sandler, M., Lees, A. J., Phuapradit, P., Shaw, K. M., Stern, G. M., and Kumar, P., 1978, Deprenyl administration in man: a selective monoamine oxidase B inhibitor without the “cheese effect,” Psychopharmacology 57: 33.PubMedCrossRefGoogle Scholar
  36. Gerstenbrand, F., Ransmayr, G., and Poewe, W., 1983, Deprenyl (selegiline) in combination treatment of Parkinson’s disease. Acta Neurol. Scand. 95 (Suppl.): 123.CrossRefGoogle Scholar
  37. Ghose, K., Turner, P., and Coppen, A., 1975, Intravenous tyramine pressor response in depression, Lancet 1: 1317.PubMedCrossRefGoogle Scholar
  38. Gilman, A., Goodman, L. S., and Gilman, A., 1980, Goodman and Gilman’s The Pharmacological Basis of Therapeutics, p. 429, Macmillan, New York.Google Scholar
  39. Glover, V., Sandler, M., Owen, V., and Riley, G., 1977, Dopamine is a monoamine oxidase B substrate in man, Nature 265: 80.PubMedCrossRefGoogle Scholar
  40. Glowinski, J., and Iversen, L. L., 1966, Regional studies of catecholamines in the rat brain. I. The disposition of 3H-norepinephrine, 3H-dopamine and 3H-DOPA in various regions of the brain, J. Neurochem. 13: 655.PubMedCrossRefGoogle Scholar
  41. Hallman, H., Olson, L., and Jonsson, G., 1984, Neurotoxicity of the meperidine analogue, Nmethyl-4–phenyl-1,2,3,6–tetrahydropyridine on brain catecholamine neurons in the mouse, Eur. J. Pharmacol. 97: 133.PubMedCrossRefGoogle Scholar
  42. Harsing, L. G., Jr., Magyar, K., Tekes, K., Vizi, E. S., and Knoll, J., 1979, Inhibition by deprenyl of dopamine uptake in rat striatum: A possible correlation between dopamine uptake and acetylcholine release inhibition, Pol. J. Pharmacol. Pharm. 31: 297.PubMedGoogle Scholar
  43. Hassler, R., 1938, Zur Pathologie der Paralysis agitans und des postencephalitischen Parkinsonismus, J. Psychol. Neurol. (Lpz.) 48: 387.Google Scholar
  44. Heikkila, R. E., Hess, A., and Duvoisin, R. C. 1984, Dopaminergic neurotoxicity of 1–methyl-4phenyl-1,2,5,6–tetrahydropyridine in mice, Science 224: 1451.PubMedCrossRefGoogle Scholar
  45. Hunter, K. R., Boakes, A. J., Laurence, D. R., and Stern, G. M., 1970, Monoamine oxidase inhibitors and 1–dopa, Br. Med. J. 3: 388.PubMedCrossRefGoogle Scholar
  46. Johnston, J. P., 1968, Some observations upon a new inhibitor of monoamine oxidase brain tissue, Biochem. Pharmacol. 17: 1285.PubMedCrossRefGoogle Scholar
  47. Karoum, F., Chuang, L.-W., Eisler, T., Caine, D. B., Leibowitz, M. R., Quitkin, F. M., Klein, D. F., and Wyatt, R. J., 1982, Metabolism of (—)deprenyl to amphetamine and metamphetamine may be responsible for deprenyl’s therapeutic benefit: A biochemical assessment, Neurology 32: 503.PubMedGoogle Scholar
  48. Kerecsen, L., Kalasz, H., Tarcali, J., Fekete, J., and Knoll, J., 1985, Measurement of DA and DOPAC release from rat striatal preparations “in vitro” using HPLC with electrochemical detection, in: Chromatography, the State of the Art ( H. Kalasz and L. S. Ettre, eds.), pp. 195–203, Akademiai Kiado, Budapest.Google Scholar
  49. Kissinger, P. T., Craig, S. B., and Shoup, R. E., 1981, Neurochemical applications of liquid chromatography with electrochemical detection, Life Sci. 28: 455.PubMedCrossRefGoogle Scholar
  50. Knoll, J., 1976, Analysis of the pharmacological effects of selective monoamine oxidase inhibitors, in: Monoamine Oxidase and Its Inhibition G. E. W. Wolstenholme and J. Knight, eds.), pp. 135–161, Ciba Foundation Symposium 39 (new series) Elsevier-Excerpta Medica, North-Holland, Amsterdam.Google Scholar
  51. Knoll, J., 1978a, The pharmacology of selective irreversible monoamine oxidase inhibitors, in: Enzyme-Activated Irreversible Inhibitors ( N. Seiler, M. J. Jung and J. Koch-Weser, eds.) pp. 253–269, Elsevier North Holland Biomedical Press, Amsterdam, New York, Oxford.Google Scholar
  52. Knoll, J., 1978b, On the dual nature of monoamine oxidase, Horizons Biochem. Biophys. 5: 37.Google Scholar
  53. Knoll, J., 1978c, The possible mechanism of action of (—)deprenyl in Parkinson’s disease, J. Neural Transm. 43: 117.CrossRefGoogle Scholar
  54. Knoll, J., 1979a, Deprenyl, the MAO inhibitor without the “cheese effect,” Trends in Neurosciences 2:111.CrossRefGoogle Scholar
  55. Knoll, J., 1979b, Structure-activity relationship of the selective inhibitors of MAO-B, in: Monoamine Oxidase: Structure, Function and Altered Functions ( T. P. Singer, R. W. von Korff, and D. L. Murphy, eds.) pp. 431–446, Academic Press, New York.Google Scholar
  56. Knoll, J., 1980, Monoamine oxidase inhibitors: Chemistry and pharmacology, in: Enzyme Inhibitorsas Drugs ( M. Sandler, ed.), pp. 151–272, The Macmillan Press Ltd, London.Google Scholar
  57. Knoll, J., 1981, The pharmacology of selective MAO inhibitors, in: Monoamine Oxidase Inhibi-tors-The State of the Art ( M. B. H. Youdim and E. S. Paykel, eds.), pp. 45–61, Wiley, New York.Google Scholar
  58. Knoll, J., 1982, Selective inhibition of B type monoamine oxidase in the brain: a drug strategy to improve the quality of life in senescence, in: Strategy in Drug Research ( J. A., KeverlingBuisman, ed.) pp. 107–135, Elsevier, Amsterdam.Google Scholar
  59. Knoll, J., 1983, Deprenyl (selegiline): The history of its development and pharmacological action, Acta Neurol. Scand. 95 (Suppl.): 57.CrossRefGoogle Scholar
  60. Knoll, J., and Magyar, K., 1972, Some puzzling effects of monoamine oxidase inhibitors, Adv. Biochem. Psychopharmacol. 5: 393.PubMedGoogle Scholar
  61. Knoll, J., Ecsery, Z., Nievel, J. G., and Knoll, B., 1964, Phenylisopropil-methylpropynilamin HCI, E-250, egy uj hataspektrumu pszichoenergetikum, MTA V. Oszt. Kozl. 15: 231.Google Scholar
  62. Knoll, J., Ecsery, Z., Kelemen, K., Nievel, J. G., and Knoll, B., 1965, Phenylisopropyl-methylpropinylamine (E-250): A new spectrum psychic energizer, Arch. Int. Pharmacodyn. Ther., 155: 154.PubMedGoogle Scholar
  63. Knoll, J., Vizi, E. S., and Somogyi, G., 1967, A phenylisopropylmethylpropynilamine (E-250) tyraminantagonista hatasa, MTA V. Oszt Kozl. 18: 31.Google Scholar
  64. Knoll, J., Vizi, E. S., and Somogyi, G., 1968, Phenylisopropyl-methylpropinylamine (E-250): A monoamine oxidase inhibitor antagonizing the effects of tyramine, Arzneimittel-Forsch. 18: 109.Google Scholar
  65. Knoll, J., Yen, T. T., and Dallo, J., 1983, Long-lasting, true aphrodisiac effect of (-)deprenyl in sexually sluggish old male rats, Mod. Probi. Pharmacopsychiatry 19: 135.Google Scholar
  66. Kolata, G., 1983, Monkey model of Parkinson’s disease, Science 220: 705.PubMedCrossRefGoogle Scholar
  67. Langston, J. M., and Ballard, P. Jr., 1983, Parkinson’s disease in a chemist working with 1–methyl4–phenyl-1,2,5,6–tetrahydropyridine, N. Engl. J. Med. 309: 310.PubMedGoogle Scholar
  68. Langston, J. M., Ballard, P. Jr., Tetrud, J. W., and Irwin, I., 1983, Chronic parkinsonism in humans due to a product of meperidineanalog synthesis, Science 219: 979.PubMedCrossRefGoogle Scholar
  69. Langston, J. M., Irwin, I., and Langston, E. B., 1984, Pargyline prevents MPTP-induced parkinsonism in primates, Science 225: 1480.PubMedCrossRefGoogle Scholar
  70. Lees, A. J., Shaw, K. M., Kohout, L. J., Stern, G. M., Elsworth, J. D., Sandler, M., and Youdim, M. B. H., 1977, Deprenyl in Parkinson’s disease, Lancet 2: 791.PubMedCrossRefGoogle Scholar
  71. Magyar, K., Skolnik, J., and Knoll, J., 1971, Radiopharmacological analytic studies with deprenyl-C14, in: V. Conferentia Hungaric pro Therapia et Investigatione in Pharmacologia ( E. P. Leszkovszky, ed.), pp. 103–109, Akademiai Kiado, Budapest.Google Scholar
  72. Martilla, R., 1974, Epidemiological, Clinical and Virus-Serological Studies of Parkinson’s Disease, Thesis, Reports from the Department of Neurology, University of Turku, Finland.Google Scholar
  73. Martilla, R. J., 1980, Etiology of Parkinson’s disease, in: Parkinson’s Disease. Current Progress, Problems and Management (U. K. Rinne, M. Klinger, and G. Stamm, eds.), pp. 3–15, Elsevier North Holland Biomedical Press, Amsterdam-New York.Google Scholar
  74. Mendis, N., Pare, C. M. P., Sandler, M., Glover, V., and Stern, G., 1981, Failure of the selective monoamine oxidase B inhibitor, (-)deprenyl to alleviate depression: relationship to tyramine insensitivity? in: Monoamine Oxidase Inhibitors. The State of the Art ( M. B. H. Youdim and E. S. Paykel, eds.), pp. 171–176, John Wiley and Sons Ltd., Chichester-New York-BrisbaneToronto.Google Scholar
  75. Mytilineou, C., and Cohen, G., 1984, 1–Methyl-4–phenyl-1,2,3,6–tetrahydropyridine destroys dopamine neurons in explants of rat embryo mesencephalon, Science 225: 529.Google Scholar
  76. Pare, C. M. B., Sandler, M., and Stern, G., 1978, Clinical usefulness ofdeprenyl-A new M.A.O.I., 11th CINP Congress. Vienna, abstract, p. 286.Google Scholar
  77. Parsons, B., and Rainbow, T. C., 1984, High-affinity binding sites for 3H-MPTP may correspond to monoamine oxidase, Eur. J. Pharmacol. 102: 375.PubMedCrossRefGoogle Scholar
  78. Pollock; M., and Hornabrook, R. W., 1966, The prevalence, natural history and dementia of Parkinson’s disease, Brain 89: 429.CrossRefGoogle Scholar
  79. Portin, R., and Rinne, U. K., 1980, Neuropsychological responses of parkinsonian patients to longterm levodopa treatment, in: Parkinson’s Disease. Current Progress, Problems, and Management ( U. K. Rinne, M. Klinger, and G. Stamm, eds.), pp. 271–304, Elsevier/North Holland Biomedical Press, Amsterdam, New York.Google Scholar
  80. Portin, R., and Rinne, U. K., 1983, The effect of deprenyl (Selegiline) on cognition and emotion in parkinsonian patients undergoing long-term levodopa treatment, Acta Neurol. Scand. 95 (Suppl.): 135.CrossRefGoogle Scholar
  81. Presthus, J., and Hajba, A., 1983, Deprenyl (selegiline) combined with levodopa and a decarboxylase inhibitor in the treatment of Parkinson’s disease, Acta Neurol. Scand. 95 (Suppl.): 127.CrossRefGoogle Scholar
  82. Reynolds, G. P., Elsworth, J. D., Blau, K., Sandler, M., Lees, A. J., and Stern, G. M., 1978, Deprenyl is metabolized to methamphetamine and amphetamine in man, Br. J. Clin. Pharmacol. 6: 542.PubMedGoogle Scholar
  83. Riederer, P., Youdim, M. B. H., Birkmayer, W., and Jellinger, K., 1978, Monoamine oxidase activity during (-)deprenyl therapy: Human brain post mortem studies, in: Advances in Biochemistry and Pharmacology, 19 ( P. J. Roberts and L. L. Iversen, Eds.), pp. 377–382, Raven Press, New York.Google Scholar
  84. Rinne, U. K., 1980a, Levodopa in combination with an extracerebral decarboxylase inhibitor, in: Parkinson’s Disease. Current Progress, Problems and Management ( U. K. Rinne, M. Klinger, and G. Stamm, eds.), pp. 323–334, Elsevier/North Holland Biomedical Press, Amsterdam, New York.Google Scholar
  85. Rinne, U. K., 1980b, Long-term L-deprenyl treatment of on-off phenomena in Parkinson’s disease, in: Monoamine Oxidases and Their Selective Inhibition ( K. Magyar ed.), pp. 145–149, Pergamon Press-Akademiai Kiado, Budapest.Google Scholar
  86. Rinne, U. K. (ed.), 1983, A New Approach to the Treatment of Parkinson’s Disease, Acta Neurol. Scand. 95(Suppl.):144.Google Scholar
  87. Rinne, U. K., Sonninen, V., and Siirtola, T., 1970, L-Dopa treatment in Parkinson’s disease, Eur. Neurol. 4: 348.PubMedCrossRefGoogle Scholar
  88. Rinne, U. K., Siirtola, T., and Sonninen, V., 1978, L-deprenyl treatment of on-off phenomena in Parkinson’s disease, J. Neural Transm. 43: 253.PubMedCrossRefGoogle Scholar
  89. Sandler, M., Glover, V., Ashford, A., and Stern, G. M., 1978, Absence of “cheese effect” during deprenyl therapy: Some recent studies, J. Neural Transm. 43: 209.PubMedCrossRefGoogle Scholar
  90. Simpson, L. L., 1978, Evidence that deprenyl a type B monoamine oxidase inhibitor, is an indirectly acting sympathomimetic amine, Biochem. Pharmacol. 27: 1591.PubMedCrossRefGoogle Scholar
  91. Squires, R. F., 1972, Multiple forms of monoamine oxidase in intact mitochondria as characterized by selective inhibitors and thermal stability: A comparison of eight mammalian species. Adv. Biochem. Psychopharmacol. 5: 355.PubMedGoogle Scholar
  92. Stern, G. M., 1980, Current adjuvants to levodopa therapy, in: Parkinson’s Disease. Current Progress, Problems and Management ( U. K. Rinne, M. Klinger, and G. Stamm, eds.), pp. 357–361, Elsevier/North Holland Biomedical Press, Amsterdam, New York.Google Scholar
  93. Stern, G. M., Lees, A. J., and Sandler, M., 1978, Recent observations on the clinical pharmacology of (-)deprenyl, J. Neural Transm. 43: 245.PubMedCrossRefGoogle Scholar
  94. Stern, G. M., Lander, C. M., Lees, A. J., and Ward, C., 1982, Deprenyl, in: Rose and Capildeo Research Progress in Parkinson’s Disease, pp. 324–344, Pitman Medical, London.Google Scholar
  95. Tozer, T. N., Neff, N. H., and Brodie, B. B., 1966, Application of steady-state kinetics to the synthesis rate and turnover time of serotonin in the brain of normal and reserpine treated rats, J. Pharmacol. Exp. Ther. 153: 177.Google Scholar
  96. Tretiakoff, C., 1919, Contribution a l’etude de l’anatomie pathologique du locus niger de Sommering avec quelques deductions relatives a la pathogenie des troubles du tonus musculaire et de la maladie de Parkinson. These med. no. 293, Paris.Google Scholar
  97. Varga, A., and Tringer, L., 1967, Clinical trial of a new type of promptly acting psychoenergetic agent (phenyl-isopropyl-methyl-propinylamine HCI) (E-250), Acta Med. Acad. Sci. Hung. 23: 289.PubMedGoogle Scholar
  98. Vizi, E. S., Harsing, L. G., and Knoll, J., 1977, Presynaptic inhibition leading to disinhibition of acetylcholine release from interneurons of the caudate nucleus: effects of dopamine, β–endorphin and D-Ala2–Pro5–enkephalinamide, Neuroscience 2: 953.CrossRefGoogle Scholar
  99. Wajsbort, J., and Youdim, M. B. H., 1980, The action of L-deprenyl in L-dopa treated parkinsonian patients, with special reference to the “on-off” effect, in: Monoamine Oxidases and Their Selective Inhibition ( K. Magyar, ed.), pp. 139–144, Pergamon Press-Akademiai Kiado, Budapest.Google Scholar
  100. Yahr, M. D., 1978, Overview of present day treatment of Parkinson’s disease, J. Neural Transm. 43: 227.PubMedCrossRefGoogle Scholar
  101. Yahr, M. D., 1980, Pharmaco-therapy of parkinsonism, in: Monoamine Oxidases and Their Se-lective Inhibition ( K. Magyar, ed.), pp. 117–125, Pergamon Press-Akademiai Kiado, Budapest.Google Scholar
  102. Yahr, M. D., Duvoisin, R. C., and Shear, M. J., 1969, Treatment of parkinsonism with levodopa, Arch. Neurol. (Chicago) 21: 343.CrossRefGoogle Scholar
  103. Yahr, M. D., Mendoza, M. R., Moros, D., Bergmann, K. J., 1983, Treatment of Parkinson’s disease in early and late phases. Use of pharmacological agents with special reference to deprenyl/ selegiline, Acta Neurol. Scand. 95 (Suppl.): 95.CrossRefGoogle Scholar
  104. Ziering, A., Berger, L., Heineman, S. D., and Lee, J., 1947, Piperidine derivatives. Part III. 4Arylpiperidines, J. Org. Chem. 12: 894.PubMedCrossRefGoogle Scholar
  105. Zsilla, G., and Knoll, J., 1982, The action of (—)deprenyl on monoamine turnover rate in rat brain, in: Typical and Atypical Antidepressants ( E. Costa and G. Racagni, eds.), pp. 211–217, Raven Press, New York.Google Scholar
  106. Zsilla, G., Barbaccia, M. L., Gandolfi, O., Knoll, J., and Costa, E., 1983, (—)Deprenyl a selective MAO-B inhibitor increases H-imipramine binding and decreases j3–adrenergic receptor function, Eur. J. Pharmacol. 89: 111.PubMedCrossRefGoogle Scholar
  107. Zsilla, G., Foldi, P., Held, G., Szekely, A. M., and Knoll, J., 1986, The effect of repeated doses of (—)deprenyl on the dynamics of monoaminergic transmission. Comparison with clorgyline, Pol. J. Pharmacol. Pharm. 86.Google Scholar

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© Plenum Publishing Corporation 1986

Authors and Affiliations

  • Joseph Knoll
    • 1
  1. 1.Department of PharmacologySemmelweis University of MedicineBudapestHungary

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