Do MAO-B Inhibitors Have Any Role in the Treatment of Depression?

Part of the Milestones in Drug Therapy book series (MDT)


Parkinson’s disease (PD) is clearly associated with changes in affective state and a higher frequency of depression. Depressive symptoms have been found in about 70% of cases of PD [1], while depression that meets diagnostic criteria and significance is seen in about 40% of PD patients [2]. There is no single type of depression in PD, but rather there are several different depressive syndromes related to the nature of the PD. Mayeux et al. [3] described depressed PD patients with sleep disturbances, fatigue, psychomotor retardation, and difficulty in concentrating as dominant complaints. Schiffer et al. [4] reported atypical depression with anxiety and panic disorder to be found significantly more frequently among patients with PD. According to Starkstein et al. [5], depressed patients with PD reported a significantly higher frequency of worrying, loss of interest, hopelessness, loss of appetite and libido, as well as anxiety, i.e., they showed a predominance of autonomic and affective symptoms. Interestingly, these authors found anergia and motor retardation to be not significantly more frequent in PD patients with depression. In recent years controlled studies have provided evidence that monoamine oxidase inhibitors (MAOIs) are effective antidepressants and comparable to (tricyclic) reuptake inhibitors.


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  1. [1]
    Brown RG, MacCarthy B. Psychiatric morbidity in patients with Parkinson’s disease. Psychol Med 1990; 20: 77–87.CrossRefGoogle Scholar
  2. [2]
    Ring HA, Trimble MR. Affective disturbance in Parkinson’s disease. Int J Geriatr Psychiatry 1991; 6: 385–393.CrossRefGoogle Scholar
  3. [3]
    Mayeux R, Stern Y, Williams JBW, Cote L, Frantz A, Dyrenfurth I. Clinical and biochemical features of depression in Parkinson’s disease. Am J Psychiatry 1986; 143: 756–759.Google Scholar
  4. [4]
    Schiffer RB, Kurlan R, Rubin A, Boer S. Evidence for atypical depression in Parkinson’s disease. Am J Psychiatry 1988; 145: 1020–1024.Google Scholar
  5. [5]
    Starkstein SE, Preziosi TJ, Forrester AW, Robinson RG. Specificity of affective and autonomic symptoms of depression in Parkinson’s disease. J Neurol Neurosurg Psychiatry 1990; 53: 869–873.CrossRefGoogle Scholar
  6. [6]
    Pare CMB. The present status of monoamine oxidase inhibitors. Br J Psychiatry 1985; 146: 576–584.CrossRefGoogle Scholar
  7. [7]
    Laux G, Riederer P, editors. Clinical approaches to moclobemide, a new reversible inhibitor of MAO-A (RIMA). Psychiat Prax Suppl 1990; 17: 1–30.Google Scholar
  8. [8]
    Riederer P, Przuntek H, editors. MAO-B-inhibitor selegiline (R-(-)-deprenyl). A new therapeutic concept in the treatment of Parkinson’s disease. J Neural Transm 1987 (Supplement 25): 1–197.Google Scholar
  9. [9]
    Mann JJ, Gershon S. l-Deprenyl: a selective monoamine oxidase type B inhibitor in endogenous depression. Life Sci 1980; 26: 877–882.CrossRefGoogle Scholar
  10. [10]
    Overall JE. Efficacy of nomifensine in different depressive syndromes. J Clin Psychiatry 1984; 45 (Sect. 2): 85–88.Google Scholar
  11. [11]
    Aylward M, Maddock J, Dewland PM, Lewis PA. Sulpiride in depressive illness. Adv Biol Psychiat 1981; 7: 154–165.Google Scholar
  12. [12]
    Zsilla G, Barbaccia ML, Gandolfi O, Knoll J, Costa E. (—)-Deprenyl, a selective MAO-B inhibitor increased 3H-imipramine binding and decreased beta-adrenergic receptor function. Eur J Pharmacol 1983; 11: 117.Google Scholar
  13. [13]
    Wolfe N, Katz DI, Albert ML, Almozlino A, Durso R, Smith MC, Volicer L. Neuropsychological profile linked to low dopamine in Alzheimer’s disease, major depression, and Parkinson’s disease. J Neurol Neurosurg Psychiatry 1990; 53: 915–11917.CrossRefGoogle Scholar
  14. [14]
    Mendis N, Pare CMB, Sandler M, Glover V, Stern M. Is the failure of (—)-deprenyl, a selective monoamine oxidase B inhibitor, to alleviate depression related to freedom from the cheese effect? Psychopharmacology 1981; 73: 87–90.CrossRefGoogle Scholar
  15. [15]
    Mann JJ, Frances A, Kaplan RD, Kocsis J, Peselow ED, Gershon S. The relative efficacy of 1-deprenyl: a selective monoamine type B inhibitor, in endogenous and nonendogenous depression. J Clin Psychopharmacol 1982; 2: 54–57.CrossRefGoogle Scholar
  16. [16]
    Mendlewicz J, Youdim MBH. l-Deprenyl: a selective monoamine oxidase type B inhibitor, in the treatment of depression: a double-blind evaluation. Br J Psychiatry 1983; 142: 508–511.CrossRefGoogle Scholar
  17. [17]
    Quitkin FM, Liebowitz MR, Stewart JW, McGrath PJ, Harrison W, Rabkin JG, Markowitz J, Davies SO. l-Deprenyl in atypical depression. Arch Gen Psychiatry 1984; 41: 777–781.CrossRefGoogle Scholar
  18. [18]
    Ceskova E, Svestka J, Nahunek K, Rysanek R, Peska I, Novotna H. Clinical experience with l-deprenyl in endogenous depression. Activ Nerv Sup (Praha) 1986; 28: 47.Google Scholar
  19. [19]
    Mann JJ, Aarons SF, Wilner PJ, Keilp JG, Sweeney JA, Pearlstein T et al. A controlled study of the antidepressant efficacy and side effects of (—)-deprenyl. Arch Gen Psychiatry 1989; 46: 45–50.CrossRefGoogle Scholar
  20. [20]
    McGrath PJ, Stewart JW, Harrison W, Wager S, Nunes EN, Quitkin FM. A placebo-controlled trial of l-deprenyl in atypical depression. Psychopharmacol Bull 1989; 25: 63–67.Google Scholar
  21. [21]
    Mendlewicz J, Youdim MBH. Antidepressant potentiation of 5-hydroxytryptophan by l-Deprenyl in affective illness. J Affect Disord 1980; 2: 137–146.CrossRefGoogle Scholar
  22. [22]
    Birkmayer W, Riederer P, Linauer W, Knoll J. l-deprenyl plus l-phenylalanine in the treatment of depression. J Neural Transm 1984; 59: 81–87.CrossRefGoogle Scholar
  23. [23]
    Sabelli HC. Rapid treatment of depression with selegiline-phenylalanine combination. J Clin Psychiatry 1991; 52: 137.Google Scholar
  24. [24]
    Sheehan DV, Davidson J, Manschreck T, Van Wyck Fleet J. Lack of efficacy of a new antidepressant (bupropion) in the treatment of panic disorder with phobias. J Clin Psychopharmacol 1983; 3: 28–31.Google Scholar
  25. [25]
    Karoum F, Chuang LW, Eisler T. Metabolism of (—)-deprenyl to amphetamine and metamphetamine may be responsible for deprenyFs therapeutic benefit: a biochemical assessment. Neurology 1982; 32: 503–509.CrossRefGoogle Scholar

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© Springer Basel AG 1993

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  • G. Laux

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