Zusammenfassung
MAO-B-Hemmer inhibieren per definitionem die Aktivität des Enzyms Monoaminoxidase (MAO) Typ B durch Konkurrenz mit dem spezifischen Substrat. Entsprechend der Reversibilität der Hemmung unterscheidet man:
-
1.
kompetitive, reversible und
-
2.
irreversible Inhibitoren.
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
Literatur
Benakis (1985) Pharmacokinetic and metabolic data of Jumex® in human volunteers. In: Marton J, Zak F, Szebeni R (eds) Proceedings of the International Symposium on (-)-Deprenyl, Jumex®. Chinoin Pharmaceutical and Chemical Works, Budapest, pp 33–37
Bieck PR (1989) Hypertensive Krisen unter reversiblen Hemmstoffen der Monoaminoxidase? Ergebnisse von Tyramin-Interaktionsstudien. In: Laux G, Riederer P (Hrsg) Neue selektive Monoaminoxidase-Hemmer in der Therapie depressiver Erkrankungen. Psychiatr Prax 16: 25–31
Birkmayer WP, Riederer P, Linauer W, Knoll J (1984) L-Deprenyl plus L-phenylalanine in the treatment of depression. J Neural Transm 59: 81–87
Birkmayer W, Knoll J, Riederer P, Youdim MBH, Hars V, Marton J (1985) Increased life expectancy resulting from addition of L-deprenyl to Madopar® treatment in Parkinson’s disease: a longterm study. J Neural Transm 64: 113–127
Biackwell B, Marley E (1966) Interactions of cheese and of its constituents and monoamine oxidase inhibitors. Br J Pharmacol 26: 120–141
Cohen G (1986) Monoamine oxidase, hydrogen peroxide, and Parkinson’s disease. In: Yahr MD, Bergmann KJ (eds) Advances in neurology, vol 45 . Raven Press, New York, pp 119–125
Cohen G, Psik P, Cohen B, Leist A, Mythilineou C, Yahr MD (1984) Pargyline and deprenyl prevent the neurotoxicity of 1-methyl-4-phenyl1,2,3–6-tetrahydropyridine (MPTP) in monkeys. Eur J Pharmacol 106: 209–210
Danielczyk W, Streifler M, Konradi C, Riederer P, Moll G (1989) Platelet MAO-B activity and the psychopathology of Parkinson’ disease, senile dementia and multi-infarct dementia. Acta Psychiatr Scand 78: 730–736
Da Prada M, Kettler R, Zurcher G, Keller HH (1988) Hemmer der MAO-B und COMT: Möglichkeiten ihrer Anwendung bei der Parkinson-Therapie aus heutiger Sicht. In: Fischer PA (Hrsg) Modifizierende Faktoren bei der ParkinsonTherapie. Editiones Roche, Basel, S 309–323
Eisler T, Teravainen H, Nelson R et al. (1981) Deprenyl in Parkinson’s disease. Neurology 31: 19–23
Ekstedt B, Magyar K, Knoll J (1979) Does the B form selective monoamine oxidase inhibitor lose selectivity by long term treatment? Biochem Pharmacol 28: 919–923
Elsworth JD, Glover V, Reynolds GP et al. (1978) Deprenyl administration in man: selective monoamine oxidase B inhibitor without the “cheese effect”. Psychopharmacology 57: 33–38
Finberg J PM, Tenne M (1982) Relationship between tyramine potentiation and selective inhibition of monoamine oxidase types A and B in the rat vas deferens. Br J Pharmacol 77: 13–21
Fowler JS, Mcgregor RR, Wolf AP et al. (1987) Mapping human brain monoamine oxidase A and B with 11C-labeled suicide inactivators and PET. Science 235: 481–485
Golbe LI (1988) Deprenyl as symptomatic therapy in Parkinson’s disease. Clin Neuropharmacol 11: 387–400
Heikkila RL, Manzino L, Cabbat FS, Duvoisin RC (1984) Protection against the dopaminergic neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine by monoamine oxidase inhibitors. Nature 311: 467–469
Johnston P (1968) Some observations upon a new inhibitor of monoamine oxidase in brain tissue. Biochem Pharmacol 17: 1285–1297
Kalir A, Sabbagh A, Youdim MBH (1981) Selective acetylenic ‘suicide’ and reversible inhibitors of monoamine oxidase types A and B. Br J Pharmacol 73: 55–64
Karoum F, Chuang LW, Eisler T, Calne DB, Leibowitz MR, Quitkin FM, Klein DF, Wyatt RJ (1982) Metabolism of (-)-deprenyl to amphetamine and methamphetamine may be responsible for deprenyl’s therapeutic benefit: a biochemical assessment. Neurology 32: 503–509
Keller HH, Kettler R, Keller G, Da Prada M (1987) Short-acting novel MAO inhibitors: in vitro evidence for the reversibility of MAO inhibition by moclobemide and Ro 16–6491. Naunyn-Schmiedebergs Arch Pharmacol 335: 15–20
Knoll J (1976) Analysis of the pharmacological effects of selective monoamine oxidase inhibitors. In: Wolstenholme GEW, Knight J (eds) Monoamine oxidase and its inhibition. Elsevier/North-Holland, Amsterdam, pp 131–161 (Ciba Foundation Symposium 39)
Knoll J (1978) The possible mechanism of action of (-)deprenyl in Parkinson’s disease. J Neural Transm 43: 177–198
Knoll J (1983) Deprenyl (selegiline): the history of its development and pharmacological action. Acta Neurol Scand [Suppl] 95: 57–80
Knoll J (1986a) The pharmacology of (-)-deprenyl. J Neural Transm [Suppl] 22: 75–89
Knoll J (1986b) Role of B-type monoamine oxidase inhibition in the treatment of Parkinson’s disease. In: Shah NS, Donald HG (eds) Movement disorders. Plenum Press, New York, pp 53–81
Knoll J (1987) R-(-)-Deprenyl (Selegiline, Movergan®) facilitates the activity of the nigrostriatal dopaminergic neuron. J Neural Transm [Suppl] 25: 45–69
Knoll J, Magyar K (1972) Some puzzling effects of monoamine oxidase inhibitors. Adv Biochem Psychopharmacol 5: 393–408
Konradi C, Riederer P, Heinsen H (1989) Histochemistry of MAO subtypes in the brainstem of humans: a relation to the radical hypothesis of Parkinson’s disease? In: Przuntek H, Riederer P (eds) Early diagnosis and preventive therapy in Parkinson’s disease. Springer, Wien New York, pp 243–249
Kopin IJ (1986) Toxins and Parkinson’s disease MPTP parkinsonism in humans and animals. In: Yahr MD, Bergmann KJ (eds) Advances in neurology, vol 45. Raven Press, New York, pp 137–144
Lee DH, Mendoza M, Dvorozniak MT, Chung E, Van Woert MH, Yahr MD (1989) Platelet monoamine oxidase in Parkinson patients: effect of L-deprenyl therapy. J Neural Transm [P-DSect] 1: 189–194
Mendlewicz J, Youdim MBH (1983) L-Deprenyl, a selective monoamine oxidase type B inhibitor in the treatment of depression: a double blind evaluation. Br J Psychiatry 142: 507–511
Oreland L, Johansson F, Ekstedt J (1983) Dose regimen of deprenyl (selegiline) and platelet MAO activities. Acta Neurol Scand [Suppl] 95: 87–89
Reynolds GP, Elsworth JD, Blau K, Sandler M, Lees AJ, Stern GM (1978) Deprenyl is metabolized to methamphetamine and amphetamine in man. Br J Clin Pharmacol 6: 542–544
Riederer P, Youdim MBH (1986) Monoamine oxidase activity and monoamine metabolism in brains of parkinsonian patients treated with L-deprenyl. J Neurochem 46: 1359–1365
Riederer P, Przuntek H (1988) Morbus Parkinson — Selegilin (R-(-)-Deprenyl, Movergan®). Ein neues Therapiekonzept. Springer, Wien New York
Riederer P, Youdim MBH, Rausch WD, Birkmayer W, Jellinger K, Seemann D (1978) On the mode of action of L-deprenyl in the human central nervous system. J Neural Transm 43: 217–226
Riederer P, Jellinger K, Seemann D (1984) Monoamine oxidase and parkinsonism. In: Tipton K, Dostert P, Strolin-Benedetti M (eds) Monoamine oxidase and disease. Academic Press, London Orlando San Diego, pp 404 415
Riederer P, Konradi C, Hebenstreit G (1989) Neurochemische Perspektiven zur Funktion der Monoaminoxidase. Psychiatr Prax 16 [Suppl]: 7–11
Squires R (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: 355–370
Stern Y (1990) MPTP-induced parkinsonism. Prog Neurobiol 34: 107–114
Stern GM, Lees AJ, Hardie RJ, Sandler M (1983) Clinical and pharmacological problems of deprenyl (selegiline) treatment in Parkinson’s disease. Acta Neurol Scand [Suppl] 95: 113–116
Tetrud J, Langston W (1989) The effect of deprenyl (Selegiline) on the natural history of Parkinson’s disease. Science 245: 519–522
Tipton KF, Mantle TJ (1981) Inhibition of rat liver monoamine oxidase by clorgyline and deprenyl. In: Youdim MBH, Paykel ES (eds) Monoamine oxidase inhibitors: the state of the art. Wiley, Chichester, pp 3–27
Youdim MBH, Finberg JPM (1986) MAO Type B inhibitors as adjunct to L-DOPA therapy. In: Yahr MD, Bergmann KJ (eds) Advances in neurology, vol 45. Raven Press, New York, pp 127–136
Youdim MBH, Finberg JPM, Tipton KF (1988) Monoamine oxidase. In: Trendelenburg U, Weiner N (eds) Catecholamines I. Springer, Berlin Heidelberg New York Tokyo, pp 119–192 (Handbook of experimental pharmacology, vol 90/
Zreika M, Fozard JR, Dudley MW, Bey PH, McDonald IA, Palfreyman MG (1989) MDL 72,974: a potent and selective enzyme-activated irreversible inhibitor of monoamine oxidase type B with potential for use in Parkinson’s disease. J Neural Transm [PP-D-Sect] 1: 243–254
Zsiula G, Foldi P, Held G, Szekeix AM, Knoll J (1986) The effect of repeated doses of (-)deprenyl on the dynamics of monoaminergic transmission. Comparison with clorgyline. Pol Pharmacol Pharm 38: 57–67
Birkmayer W, Rederer P, Youdim MBH, 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: 303–326
Birkmayer W, Knoll J, Riederer P, Youdim MBH, Hars V, Marton J (1985) Increased life expectancy resulting from addition of L-deprenyl to madopar treatment in Parkinson’s disease: a longterm study. J Neural Transm 64: 113–127
Csanda E, Tarczy M (1987) Selegeline in the early and late phases of Parkinson’s disease. J Neural Transm [Suppl 25]: 105–113
Eisler T, Terävainen H, Nelson R, Krebs H, Weise V, Lake CR, Ebert MH, Whetzel N, Murphy DL, Kopin IJ, Calne DB (1981) Deprenyl in Parkinson’s disease. Neurology 31: 19–23
Fischer PA, Baas H (1987) Therapeutic efficacy of deprenyl as adjuvant therapy in advanced parkinsonism. J Neural Transm [Suppl 25]: 137–147
Golbe LI, Duvoisin RC (1987) Deprenyl for on-off Parkinson’s disease. J Neural Transm [Suppl 25]: 123–129
Goldstein L (1980) The “on-off’ phenomena in Parkinson’s disease. Treatment and theoretical considerations. Mt Sinai J Med 47: 80–84
Heikkila RL, Manzino L, Duvoisin RC, Cabbat FS (1984) Protection against the dopaminergic neurotoxicity of 1-methyl-4phenyl-1,2,3,6-tetrahydropyridine by monoamine oxidase inhibitors. Nature 311: 467–469
Johnston JP (1968) Some observations upon a new inhibitor of monoamine oxidase in brain tissue. Biochem Pharmacol 17: 1285–1297
Knoll J, Magyar K (1972) Some puzzling effect of monoamine oxidase inhibitors. Adv Biochem Psychopharmacol 5: 393–408
Knoll J, Vizi ES, Somogyi G (1967) Phenyliso propylmethylpropinyl-amine (E-250) tyraminantagonista hatása MTA V. Oszt Közl 18: 33–37
Laux G (1992) Do MAO-B inhibitors have any role in the treatment of depression? In: Szelenyi I (ed) Inhibitors of monoamine oxidase B. Basic and clinical aspects. Birkhäuser, Basel (in press)
Lees AJ, Shaw KM, Kohout, Stern GM, Elsworth JD, Sandler M, Youdim MBH (1977) Deprenyl in Parkinson’s disease. Lancet ii: 791–796
Mann G, Gershon S (1980) L-deprenyl, a selectice monoamine oxidase type-B inhibitor in endogenous depression. Life Sci 29: 877–882
Mylilä W, Sotaniemi KA, Tuominenj, Heinonen EH (1989) Selegiline as primary treatment in early phase Parkinson’s disease — an interim report. Acta Neurol Scand [Suppl 126]: 177–182
Parkinson Study Group (1989a) Datatop: a multicenter controlled clinical trial in early Parkinson’s disease. Arch Neurol 46: 1052–1060
Parkinson Study Group (1989b) Effect of deprenyl on the progression of disability in early parkinson’s disease. N Engl J Med 321: 1364–1371
Presthus J, Hajba A (1983) Deprenyl (selegiline) combined with levodopa and a decarboxylase inhibitor in the treatment of Parkinson’s disease. Acta Neurol Scand 68 [Suppl 95]: 127–133
Przuntek H, Kuhn W (1987) The effect of R-(-)deprenyl in de novo Parkinson patients on combination therapy with levodopa and decarboxylase inhibitor. J Neural Transm [Suppl 25]: 97–104
Reynolds GP, Riederer P, Sandler M, Jellinger K, Seemann D (1978) Amphetamine and 2-phenylethylamine in post-mortem parkinsonian brain after deprenyl administration. J Neural Transm 43: 271–277
Rinne UK (1987) R(-)-deprenyl as an adjuvant to levodopa in the treatment of Parkinson’s disease. J Neural Transm [Suppl 25]: 149–155
Stern GM, Lees AJ, Sandler M (1978) Recent observations on the clinical pharmacology of deprenyl. J Neural Transm 43: 245–251
Sunderiand T, Mueller EA, Cohen RM, Jimerson DC, Pickar D, Murphy DL (1985) Tyramine pressor sensitivity changes during deprenyl treatment. Psychopharmacology 86: 432–437
Tetrud JW, Langston JW (1989) The effect of deprenyl (selegiline) on the natural history of Parkinson’s disease. Science 245: 519–522
Ulm G, Fornadi F (1987) R-(-)-deprenyl in the treatment of end-of-dose akinesia. J Neural Transm [Suppl 25]: 163–172
Yahr MD (1989) Selegiline in the treatment of Parkinson’s disease long-term experience. Acta Neurol Scand [Suppl 126]: 157–161
Zornberg GL, Bodkin JA, Cohen BM (1991) Severe adverse interaction between pethidine and selegiline. Lancet 337: 246
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1992 Springer-Verlag Wien
About this chapter
Cite this chapter
Gerlach, M., Riederer, P., Fischer, PA. (1992). MAO-B-Hemmer. In: Riederer, P., Laux, G., Pöldinger, W. (eds) Neuro-Psychopharmaka. Springer, Vienna. https://doi.org/10.1007/978-3-7091-3330-9_6
Download citation
DOI: https://doi.org/10.1007/978-3-7091-3330-9_6
Publisher Name: Springer, Vienna
Print ISBN: 978-3-7091-3331-6
Online ISBN: 978-3-7091-3330-9
eBook Packages: Springer Book Archive