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The demonstration that the DEP analog (−)-1-phenyl-2-propylaminopentane devoid of MAO inhibitory property, enhanced like DEP the activity of the catecholaminergic brain engine revealed that this effect is unrelated to the selective inhibition of MAO-B. β-Phenylethylamine (PEA), the important trace-amine in the mammalian brain, is known to be a releaser of catecholamines. Amphetamine and methamphetamine, the best known synthetic PEA derivatives are also releasers of catecholamines like their parent compound. DEP is a unique synthetic PEA derivative devoid of the catecholamine releasing property. As the releasing effect conceals the catecholaminergic activity enhancer (CAE) effect, it remained undiscovered until DEP uncovered that PEA is a natural CAE substance; and only releases catecholamines in high concentration. Discovering that tryptamine is a natural enhancer of catecholaminergic and serotonergic neurons catalyzed the development of R-(−)-1-(benzofuran-2-yl)-2-propylaminopentane (BPAP); the most potent and selective enhancer substance, and it exerts its enhancer effect in 0.0001 mg kg-1. DEP and BPAP initiated an analysis of the enhancer regulation in the mammalian brain. Studies regarding the nature of the enhancer regulation revealed that this regulation is enhanced after weaning and sex hormones return it to the pre-weaning level. Thus, sex hormones elicit the transition of the developmental phase of life into the post-developmental, downhill (aging) period. The aging-related, slow decline in the enhancer regulation of the catecholaminergic brain engine, the main activator of the cortex, is the prime factor of brain aging. The enhancer regulation’s decay in the most rapidly aging dopaminergic system is, for example, mainly responsible for the decline in learning ability and sexual activity over time. According to the Knoll concept, based on two longevity studies performed on male rats, to keep the catecholaminergic brain engine, from the beginning of the downhill period of life, via the administration of a small daily dose of a CAE substance (presently DEP is the only available drug) on a higher activity level, thus to fight against the physiological aging-related slow decay of the catecholaminergic system, is a suitable anti-aging therapy. 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Riederer, P., Wuketich, S., Time course of nigrostriatal degeneration in Parkinson's disease (1976) J Neural Transm, 38, pp. 277-301", "listPosition" : 18, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132428, "link" : "/api/reference/2132428", "label" : "19. Fowler, C.J., Wiberg, A., Oreland, L., Winblad, B., The effect of age on the activity and molecular properties of human brain monoamine oxidase (1980) J Neural Transm, 49, pp. 1-20", "listPosition" : 19, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132429, "link" : "/api/reference/2132429", "label" : "20. McGeer, E.G., McGeer, P.L., Wada, J.K., Distribution of tyrosine hydroxylase in human and animal brain (1971) J Neurochem, 18, pp. 1647-1658", "listPosition" : 20, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132430, "link" : "/api/reference/2132430", "label" : "21. Birkmayer, W., Knoll, J., Riederer, P., Youdim, M.B., Hars, V., Marton, J., Increased life expectancy resulting from addition of L-deprenyl to Madopar treatment in Parkinson's disease: A longterm study (1985) J Neural Transm, 64, pp. 113-127", "listPosition" : 21, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132431, "link" : "/api/reference/2132431", "label" : "22. Knoll, J., Dalló, J., Yen, T.T., Striatal dopamine, sexual activity and lifespan. Longevity of rats treated with (-)deprenyl (1989) Life Sci, 45, pp. 525-531", "listPosition" : 22, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132432, "link" : "/api/reference/2132432", "label" : "23. Knoll, J., The pharmacology of selegiline /(-)deprenyl/ (1989) Acta Neurol Scand, 126, pp. 83-91", "listPosition" : 23, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132433, "link" : "/api/reference/2132433", "label" : "24. 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Tetrud, J.W., Langston, J.W., The effect of (-)deprenyl (selegiline) on the natural history of Parkinson's disease (1989) Science, 245, pp. 519-522", "listPosition" : 27, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132437, "link" : "/api/reference/2132437", "label" : "28. Effect of (-)deprenyl on the progression disability in early Parkinson's disease (1989) New Eng J Med, 321, pp. 1364-1371", "listPosition" : 28, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132438, "link" : "/api/reference/2132438", "label" : "29. Knoll, J., Pharmacological basis of the therapeutic effect of (-)deprenyl in age-related neurological diseases (1992) Med Res Rev, 12, pp. 505-524", "listPosition" : 29, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132439, "link" : "/api/reference/2132439", "label" : "30. 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Miklya, I., Knoll, B., Knoll, J., A pharmacological analysis elucidating why, in contrast to (-)-deprenyl (selegiline) α-tocopherol was ineffective in the DATATOP study (2003) Life Sci, 72, pp. 2641-2648", "listPosition" : 32, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132442, "link" : "/api/reference/2132442", "label" : "33. Miklya, I., The Knoll-concept to decrease the prevalence of Parkinson's disease, Chapter 5 (2011) Towards New Therapies for Parkinson's Disease, pp. 77-100. , Finkelstein DI (ed) InTech Open Access Publisher: Rijeka, Croatia", "listPosition" : 33, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132443, "link" : "/api/reference/2132443", "label" : "34. Miklya, I., Essential difference between the pharmacological spectrum of (-)-deprenyl and rasagiline (2014) Pharmacol Rep, 66, pp. 453-458", "listPosition" : 34, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132444, "link" : "/api/reference/2132444", "label" : "35. A controlled trial of rasagiline in early Parkinson disease: The TEMPO study (2002) Arch Neurol, 59, pp. 1937-1943", "listPosition" : 35, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132445, "link" : "/api/reference/2132445", "label" : "36. Knoll, J., Tóth, V., Kummert, M., Sugár, J., (-)Deprenyl and (-)parafluorodeprenyl-treatment prevents age-related pigment changes in the substantia nigra. A TV-image analysis of neuromelanin (1992) Mech Ageing Dev, 63, pp. 157-163", "listPosition" : 36, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132446, "link" : "/api/reference/2132446", "label" : "37. Knoll, J., Miklya, I., Multiple, small dose administration of (-)deprenyl enhances catecholaminergic activity and diminishes serotoninergic activity in the brain and these effects are unrelated to MAO-B inhibition (1994) Arch Int Pharmacodyn Ther, 328, pp. 1-15", "listPosition" : 37, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132447, "link" : "/api/reference/2132447", "label" : "38. Knoll, J., Miklya, I., Enhanced catecholaminergic and serotoninergic activity in rat brain from weaning to sexual maturity. Rationale for prophylactic (-)deprenyl (selegiline) medication (1995) Life Sci, 56, pp. 611-620", "listPosition" : 38, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132448, "link" : "/api/reference/2132448", "label" : "39. Knoll, J., Miklya, I., Knoll, B., Markó, R., Rácz, D., Phenylethylamine and tyramine are mixed-acting sympathomimetic amines in the brain (1996) Life Sci, 58, pp. 2101-2114", "listPosition" : 39, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132449, "link" : "/api/reference/2132449", "label" : "40. Knoll, J., (2012) How Selegiline /(-)-Deprenyl Slows Brain Aging, , Bentham Science Publishers: E-book, Sharjah, United Arab Emirates", "listPosition" : 40, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132450, "link" : "/api/reference/2132450", "label" : "41. Martini, E., Pataky, I., Szilágyi, K., Venter, V., Brief information on an early phase-II study with (-)deprenyl in demented patients (1987) Pharmacopsychiatry, 20, pp. 256-257", "listPosition" : 41, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132451, "link" : "/api/reference/2132451", "label" : "42. 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Wilcock, G.K., Birks, J., Whitehead, A., Evans, S.J., The effect of selegiline in the treatment of people with Alzheimer's disease: A meta-analysis of published trials (2002) Int J Geriatr Psychiatry, 17, pp. 175-183", "listPosition" : 44, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132454, "link" : "/api/reference/2132454", "label" : "45. Milgram, N.W., Ivy, G.O., Head, E., Murphy, P.M., Wu, P.H., Ruehl, W.W., The effect of L-deprenyl on behavior, cognitive function, and biogenic amines in the dog (1993) Neurochem Res, 18, pp. 1211-1219", "listPosition" : 45, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132455, "link" : "/api/reference/2132455", "label" : "46. 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Knoll, J., Miklya, I., Knoll, B., Dalló, J., Sexual hormones terminate in the rat the significantly enhanced catecholaminergic/serotoninergic tone in the brain characteristic to the post-weaning period (2000) Life Sci, 67, pp. 765-773", "listPosition" : 48, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132458, "link" : "/api/reference/2132458", "label" : "49. Knoll, J., (-)Deprenyl (selegiline) a catecholaminergic activity enhancer (CAE) substance acting in the brain (1998) Pharmacol Toxicol, 82, pp. 57-66", "listPosition" : 49, "published" : false, "snippet" : true }, { "otype" : "Reference", "mtid" : 2132459, "link" : "/api/reference/2132459", "label" : "50. 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