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DeprenylWith aging, MAO (monoamine oxidases) activity increases in the human brain with potential depression inducing results. In research, some of the potential for clinical uses of the compound have been associated with directly increasing synaptic dopamine levels through MAO-B inhibition. However, many think that the compounds effects are due to the fact that the compound (and a related compound called PEA) are catecholamine activity enhancers. Catecholamines are inter-related neurotransmitters dopamine, noradrenalin, and adrenalin. Catecholamines are the transmitters for key activating brain circuits. With aging, after sexual maturity, the activity of the catecholamine nervous system gradually declines, and research has suggested that the rate of decline determines the rate at which a person or animal ages. Therefore, some researcher's believe that deprenyl's catecholamine activity enhancers effect is the explaining factor for its observed anti-aging benefits. What is also important from anti aging perspective, is that Deprenyl has been shown to protect nerve cells from neurotoxins, such as MPTP conversion to MPP+, 6-OHDA, and DSP-4. Dr Joseph Knoll, who has studied Deprenyl extensively, has suggested that the brain, especially the the nigrostriatal tract, controls maximum lifespan in humans. The nigrostriatal tract typically dies off at an average rate of 13% per decade starting around age 45 in humans and sets the technical maximum life span of humans at about 115 years of age. As Deprenyl has been suggested in research by Dr. Knoll to decrease the nigrostriatal neuron death rate, the compound may increase the human technical lifespan. Deprenyl - StudiesKnoll, J. (1983) “Deprenyl (selegeline): the history of its development and pharmacological action” Acta Neurol Scand (Suppl) 95, 57-80. 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(1996) “Selegeline in treatment of behavioral and cognitive symptoms of Alzheimer disease” Ann Pharmacother 30, 1122-29. Birkmayer, W. et al (1984) “L-deprenyl plus L-phenylalanine in the treatment of depression” J Neural Transm 59, 81-87. Sabelli, H. (1991) “Rapid treatment of depression with selegeline-phenylalanine combination” J Clin Psychiat 52,3. Knoll, J. (1997) “Sexual performance and longevity” Exp Gerontal 32, 539-52. Knoll, J. (1995) “Rationale for (-)-deprenyl (selegeline) medication in Parkinson’s disease and in prevention of age-related nigral changes” Biomed Pharmacother 49, 187-95. Ruehl, W. et al (1997) “Treatment with L-deprenyl prolongs life in elderly dogs” Life Sci 61, 1037-44. Knoll, J. (1992) “The pharmacological profile of (-)-deprenyl (selegeline) and its relevance for humans: a personal view” Parmacol Toxicol 70, 317-21. Youdim, M. & Finberg, J. (1994) “Pharmacological actions of L-deprenyl (selegeline) and other selective monoamine oxidase B inhibitors” Clin Pharmacol Ther 56, 725-33. Lange, K. et al (1994) “Biochemical actions of L-deprenyl (selegeline)” Clin Pharmacol Ther 56, 734-41. Knoll, J. et al (1996) “Phenylethylamine and tyramine are mixed-acting sympathomimetic amines in the brain” Life Sci 58, 2101-14. Finali, G. et al (1991) “L-deprenyl therapy improves verbal memory in amnesic Alzheimer patients” Clin Neuropharmacol 14, 523-36. Leonard, B. (1997) “The role of noradrenaline in depression: a review” J Psychopharmacol 11(Suppl), S39-S47. Brown, A & Gershon, S. (1993) “Dopamine and depression” J Neural Transm 91, 75-109. Knoll, J. (1994) “Memories of my 45 years in research” Pharmacol Toxicol 75, 65-72. Paterson, I. et al (1990) “2-Phenylethylamine: a modulator of catecholamine transmission in the mammalian central nervous system?” J Neurochem. 55, 1827-37. Gerlach, M. et al (1996) “Pharmacology of selegiline” Neurol 47 (Suppl), S137-S145. Knoll, J (1992) “Deprenyl-medication: a strategy to modulate the age-related decline of the striatal dopaminergic system” J Am Geriat Soc 40, 839-47. Suuronen, T. et al (2000) “Protective effect of L-deprenyl against apoptosis induced by okadaic acid in cultured neuronal cells” Biochem Pharmacol 59, 1589-95. Birkmayer, W. et al (1985) “Increased life expectancy resulting from addition of L-deprenyl to Madopar® treatment in Parkinson’s disease: a long term study: J Neural Transm 64, 113-27. Parkinson Study Group (1996) “Impact of deprenyl and tocopherol treatment on Parkinson’s disease in DATATOP subjects not requiring levodopa” Ann Neurol 39, 29-30. Lees, A (1995) “Comparison of therapeutic effects and mortality data of levodopa and levodopa combined with selegeline in patients with early, mild Parkinson’s disease” Br Med J 311, 1602 - 07. Maki-Ikola, O. et al (1996) 8 letters criticizing Lee’s 1995 study Br Med J 312, 702-04. Olanwo, C. et al (1996) “ Selegiline and mortality in Parkinson’s disease” Ann Neurol 40, 841-45. Fahn, S. (1996) “ is L-dopa toxic?” Neurol 47 (Suppl) S184-S193 Rinne, J. et al (1991) “Selegiline (deprenyl) treatment and death of migral neurons in Parkinson’s disease” Neurol 41, 859-61. Sabelli, H. et al (1986) “Clinical studies on the phenylethylamine hypothesis of affective disorder: urine and blood phenylacetic acid and phenylalanine dietary supplements” J Clin Psychiat 47,777-81. Sunderland, T. et al (1994) “High-dose selegiline in treatment-resistant older depressive patients” Arch Gen Psychiat 51, 607-15. Mann, J. et al (1989) “A controlled study of the antidepressant efficacy and side effects of deprenyl” Arch Gen Psychiat 46, 45-50.
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