Tuesday, 27.10.2020

Joseph Knoll: Enhancer Sensitive Brain Regulations and Synthetic Enhancers (Selegiline, BPAP) which Counteract the Regressive Effects of Brain Aging

 

Abbreviations and Bibliography

 

Abbreviations:

 

AD                   Alzheimer’s disease

AM                   Amphetamine

BPAP                (2R)-1-(1-benzofuran-2-yl)-N-propylpentane-2-amine   

CAE                  Catecholaminergic activity enhancer

CAR                  Conditioned avoidance response

CNS                  Central nervous system

CR                    Conditioned reflex

CS                     Conditioned stimulus

DA                     Dopamine

DATATOP           Deprenyl And Tocopherol Antioxidant Therapy Of Parkinsonism

DEP                   (R)-N-methyl-N-(1-phenylpropan-2-yl)prop-2-yn-1-amine,

                         selegiline /(-)-deprenyl (Eldepryl, Jumex, Emsam, Zelepar)

DMI                    Desmethylimipramine

ECR                    Extinguishable conditioned reflex

EF                      Escape failure

HP                      Highest performing

ICR                     Inextinguishable conditioned reflex

IPAP                   (-)-1-(indol-3-yl)-2-propylamino-pentane

IR                       Inter-trial response

LP                      Lowest performing

MAM                   Methamphetamine

MAO                   Monoamine oxidase

MAO-A                A-type monoamine oxidase

MAO-B                B-type monoamine oxidase

MDD                   Major depressive disorder

NE                     Norepinephrine

PEA                    b-phenylethylamine

PD                      Parkinson’s disease

PPAP                  (-)-1-phenyl-2-propylaminopentane

PSG                    Parkinson Study Group

SAR                    Structure-activity-relationship

SE                      Serotonin

SOD                    Superoxide-dismutase

TA                      Trace amine

TBZ                    Tetrabenazine

TLS                    Technical lifespan

TLSh                   Human technical lifespan

TMS                   tumor-manifestation-suppressing

TRY                   Tryptamine

US                     Unconditioned stimulus

VMAT2               Vesicular monoamine transporter 2

 

Bibliography

 

Chapter 1

[1] S. Dunn, (Ed.), Dachau 29 April 1945, The Rainbow Liberation Memories, Texas Tech University Press, Lubbock, Texas. 1998.

[2] J. Knoll, The theory of active reflexes. An analysis of some fundamental mechanisms of higher nervous activity, Publishing House of the Hungarian Academy of Sciences, Budapest, Hafner Publishing Company, New-York. 1969.

[3] J. Knoll, The brain and its self. A neurochemical concept of the innate and acquired drives, Springer, Berlin, Heidelberg, New-York. 2005.

[4] J. Knoll, I. Miklya, Longevity study with low doses of selegiline/(-)-deprenyl and (2R)-1-(1-benzofuran-2-yl)-N-propylpentane-2-amine (BPAP), Life Sci. 167 (2016) 32-38.

 

Chapter 2

[5] J. Knoll, K. Kelemen, B. Knoll, Experimental studies on the higher nervous activity of animals. I. A method for the elaboration of a non-extinguishable conditioned reflex in the rat, Acta Physiol. Hung. 8 (1955) 327-345.

[6] J. Knoll, K. Kelemen, B. Knoll, Experimental studies on the higher nervous activity of animals. II. Differences in the state of function of the cells constituting the cortical representation of the unconditioned reflex in extinguishable and non-extinguishable conditioned reflexes, Acta Physiol. Hung. 8 (1955) 347-367.

[7] J. Knoll, K. Kelemen, B. Knoll, Experimental studies on the higher nervous activity of animals. III. Experimental studies on the active conditioned reflex, Acta Physiol. Hung. 8 (1955) 369-388.

[8] J. Knoll, K. Kelemen, B. Knoll, Experimental studies on the higher nervous activity of animals. IV. A method for elaborating and studying an active conditioned feeding reflex. Experimental analysis of differences between active conditioned defensive and feeding reflexes, Acta Physiol. Hung. 9 (1956) 99-109.

[9] J. Knoll, Experimental studies on the higher nervous activity of animals. V. The functional mechanism of the active conditioned reflex, Acta Physiol. Hung. 10 (1956) 89-100.

[10] J. Knoll, Experimental studies on the higher nervous activity of animals. VI. Further studies on active reflexes, Acta Physiol. Hung. 12 (1957) 65-92.

[11] K. Kelemen, W.G. Longo, J. Knoll, D. Bovet, The EEG arousal reaction in rats with extinguishable and non-extinguishable conditioned reflexes, Electroencephalic Clinical Neurophysiology 13 (1961) 745-751.

[12] B. Knoll, Certain aspects of the formation of temporary connections in comparative experiments on mice and rats, Acta Physiol. Hung. 20 (1961) 265-271.

[13] B. Knoll, Comparative physiological and pharmacological analysis of the higher nervous function of mice and rats, PhD theses (in Hungarian), Hungarian Academy of Sciences, Budapest, (1968).

[14] B. Knoll, Comparative physiological examination of the working of higher nervous system in mouse and rat, Dissertation, Budapest, (1959) (in Hungarian)

[15] J. Knoll, B. Knoll, Reserpine: modification of its tranquilizer effect and analysis of its central mode of action, Arch. Int. Pharmacodyn. Ther. 133 (1961) 310-326.

[16] J. Knoll, B. Knoll, The cumulative nature of the reserpine effect and the possibilities of inhibiting cumulation pharmacologically, Arch. Int. Pharmacodyn. Ther. 148 (1964) 200-216.

[17] J. Knoll, K. Nador, B. Knoll, J. Heidt, J. Nievel, Beta-aminoketones, a new group of tranquillizers, Arch. Int. Pharmacodyn. Ther. 130 (1961) 155-169.

[18] J. Knoll, The future of mankind. Considerations on the basis of cortical mechanisms responsible for the human society’s birth and development, Budapest, Semmelweis, (2010) 329 pages (in Hungarian). inhn.org/Books September 1 (2016) with comment.

 

Chapter 3

[19] J. Knoll, Z. Ecsery, J. Nievel, B. Knoll, Phenylisopropylmethyl-propinylamine HCl (E-250) egy új hatásspektrumu pszichoenergetikum, MTA V. Oszt. Közl. 15 (1964) 231-238.  

[20] J. Knoll, Z. Ecseri, K. Kelemen, J. Nievel, B. Knoll, Phenylisopropylmethyl-propinylamine (E-250) a new psychic energizer, Arch. int. Pharmacodyn. Thér. 155 (1965) 154-164.

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[26] J. Knoll, E.S. Vizi, G. Somogyi, Phenylisopropylmethylpropinylamine (E-250), a monoamine oxidase inhibitor antagonizing the effects of tyramine, Arzneimittelforsch.  18 (1968) 109-112.

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[28] A. Abdorubo, J. Knoll, The effect of Various MAO-B inhibitors on rabbit arterial strip response to tyramine, Polish Journal of Pharmacology and Pharmacy 40 (1988) 673-683.

[29] A.R. Maass, M.J. Nimmo, A new inhibitor of serotonin metabolism, Nature 184 (1959) 547-548.

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[31] J.P. Johnston, Some observations upon a new inhibitor of monoamine oxidase in human brain, Biochem. Pharmacol. 17 (1968) 1285-1297.

[32] J. Knoll, Z. Ecsery, K. Magyar, E. Satory, Novel (-)deprenyl derived selective inhibitors of B type monoamine oxidase, The relation of structure to their action. Biochem. Pharmacol. 27 (1978) 1739-1747.

[33] P. Bey, J. Fozard, I.A. McDonald, M.G. Palfreyman, M. Zreika, MDL 72145: a potent and selective inhibitor of MAO type B, Br. J. Pharmacol. 81 (1984) 50.

[34] J.P.M. Finberg, M. Tenne, M.B.H. Youdim, Selective irreversible propargyl derivative inhibitors of monoamine oxidase (MAO) without the cheese effect, In Monoamine oxidase inhibitors-the state of the art, Eds. M.B.H. Youdim, E.S. Paykel, Whiley, Chichester, (1981) 31-44.

[35] R. Kettler, H.H. Keller, E.P. Bonetti, P.C. Wyss, M. Da Prada, Ro16-6491: A new highly selective and reversible MAO-B inhibitor (abstract), J. Neurochem. Suppl.  44 (1985) S94.

[36] E. Varga, L. Tringer, Clinical trial of a new type of promptly acting psychoenergetic agent (phenyl-isopropylmethyl-propinylamine HCl, E-250), Acta Med. Hung. 23 (1967) 289-295.

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[38] J.J. Mann, S. Gershon, A selective monoamine oxidase-B inhibitor in endogenous depression. Life Sci. 26 (1980) 877-882.

[39] J.A. Bodkin, J.K. Amsterdam, Transdermal selegiline in major depression: a double-blind, placebo-controlled, parallel-group study in outpatients, Am. J. Psych. 159 (2002) 1869-1875.

[40] J.  Knoll, Discovery of the enhancer regulation in the mammalian brain and the development of synthetic enhancer substances. A chance to significantly improve the quality and prolong the duration of human life, inhn.org URL:http://inhn.org; e-books (2016).

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[47] J. Knoll, K. Magyar, Some puzzling effects of monoamine oxidase inhibitors, Advances Biochem. Psychopharmacol. 5 (1972) 393-408.

[48] J. Knoll, (-)Deprenyl (selegiline) a catecholaminergic activity enhancer (CAE) substance acting in the brain, Pharmacology and Toxicology  82 (1998) 57-66.

[49] J. Knoll, 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. Keverling Buisman, editor). Amsterdam, Elsevier (1982) p.107-135.

[50] J. Knoll, B. Knoll, Z. Török, J. Timar, S. Yasar, The pharmacology of 1-phenyl-2-propylaminopentane (PPAP), a deprenyl-derived new spectrum psychostimulant, Arch. int. Pharmacodyn. Thér. 316 (1992) 5-29.

[51] J. Knoll, Memories of my 45 years in research. Pharmacol. Toxicol. 75 (1994) 65-72.

[52] J. Knoll, I. Miklya, 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, Arch. int. Pharmacodyn. Thér. 328 (1994) 1-15.

[53] J. Knoll, I. Miklya, B. Knoll, R. Markó, K. Kelemen, (-)Deprenyl and (-)1-phenyl-2-propylaminopentane, (-)PPAP, act primarily as potent stimulants of action potential-transmitter release coupling in the catecholaminergic neurons, Life Sci.  58 (1996) 817-827.

[54] J. Knoll, I. Miklya, B. Knoll, R. Markó, D. Rácz, Phenylethylamine and tyramine are mixed-acting sympathomimetic amines in the brain. Life Sci. 58 (1996) 2101-2114.

[55] J. Knoll, F. Yoneda, B. Knoll, H. Ohde, I. Miklya, (-)l-(Benzofuran-2-yl)-2-propylaminopentane, [(-)BPAP], a selective enhancer of the impulse propagation mediated release of catecholamines and serotonin in the brain, Br. J. Pharmacol. 128 (1999) 1723-1732.

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[58] J.M. Saavedra, Enzymatic isotopic assay for and presence of beta-phyenylathylamine in brain, J. Neurochem. 22 (1974) 211-216.

[59] J. Wilner, H.F. LeFevre, E. Costa, Assay by multiple ion detection of phenylethylamine and phenylethanolamine in rat brain, J. Neurochem. 23 (1974) 857-859.

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[62] B. Borowsky, N. Adham, K.A. Jones, R. Raddatz, R. Artymyshyn, K.L. Ogozalek, et al., Trace amines: Identification of a family of mammalian G protein-coupled receptors, Proc. Nat. Acad. Sci. USA 98 (16) (2001) 8966-8971.

[63] J. Knoll, The striatal dopamine dependency of lifespan in male rats. Longevity study with (-)deprenyl, Mech. Ageing Dev. 46 (1988) 237-262.

[64] J.W. Tetrud, J.W. Langston, The effect of (-)deprenyl (selegiline) on the natural history of Parkinson’s disease, Science  245 (1989) 519-522.

[65] Parkinson Study Group. Effect of (-)deprenyl on the progression disability in early Parkinson's disease, New Engl. J. Med. 321 (1989) 1364-1371.

[66] H. Allain, J. Gougnard, H.C. Naukirek, Selegiline in de novo parkinsonian patients: the French selegiline multicenter trial (FSMP), Acta Neurol. Scand. 136 (1991) 73-78.

[67] V.V. Myttyla, K.A. Sotaniemi, J.A. Vourinen, E.H. Heinonen, Selegiline as initial treatment in de novo parkinsonian patiens, Neurology 42 (1992) 339-343.

[68] S. Palhagen, E.H. Heinonen, J. Hagglund, T. Kaugesaar, H. Kontants, O. Mäki-Ikola, et al., Selegiline delays the onset of disability in de novo parkinsonian patients, Swedish Parkinson Study Group, Neurology 51 (2) (1998) 520-525.

[69] J.P. Larsen, J. Boas, J.E. Erdal, Does selegiline modify the progression of early Parkinson’s disease? Results from a five-year study, The Norwegian-Danish Study Group, Eur. J. Neurol. 6 (1999) 539-547.

[70] Parkinson Study Group. Effect to tocopherol and (-)deprenyl on the progression of disability in early Parkinson’s disease, New Eng. J. Med.  328 (1993) 176-183.

[71] Parkinson Study Group. Impact of deprenyl and tocopherol treatment of Parkinson’s disease in DATATOP patients requiring levodopa, Ann. Neurol. 39 (1996) 37-45.

[72] A.J. Lees, Comparison of therapeutic effects and mortality data of levodopa and levodopa combined with selegiline in patients with early, mild Parkinson’s disease.
Br. Med. J. 311 (1995) 1602-1607.

[73] S.M. Dobbs, R.J. Dobbs, A. Charlett, Multi-centre trials: U-turns by bandwagons and the patient left by the wayside, Br. J. Clin. Pharmacol. 42 (1996) 143-145.

[74] J. Knoll, (-)Deprenyl (selegiline) in Parkinson’s disease: a pharmacologist’s comment, Biomed. Pharmacother. 50 (1996) 315-317.

[75] C.W. Olanow, J.H. Godbold, W. Koller, Effect of adding selegiline to levodopa in early, mild Parkinson’s disease. Patients taking selegiline may have received more levodopa than necessary, Br. Med. J. 312 (1996) 702-703.

[76] I. Miklya, B. Knoll, J. Knoll, A pharmacological analysis elucidating why, in contrast to (-)-deprenyl (selegiline) α-tocopherol was ineffective in the DATATOP study, Life Sci.72 (2003) 2641-2648.

[77] Parkinson Study Group, A controlled trial of rasagiline in early Parkinson disease: the TEMPO study, Arch. Neurol. 59 (2002) 1937-1943.

[78] C.W. Olanow, O. Rascol, The delayed-start study in Parkinson disease: can’t satisfy everyone. Neurology 74 (2010) 1149-1150.

[79] J.E. Ahlskog, R.J. Uitti, Rasagiline, Parkinson neuroprotection, and delayed-start trials: still no satisfaction? Neurology 74 (2010) 1143-1148.

[80] B.J. Robottom, Efficacy, safety, and patient preference of monoamine oxidase B inhibitors in the treatment of Parkinson’s disease, Patient Preference and Adherence 5 (2011) 57-643.

[81] I. Miklya, Essential difference between the pharmacological spectrum of (-)-deprenyl and rasagiline, Pharmacol. Rep. 66 (2014) 453-458.

[82] J. Knoll, Pharmacological basis of the therapeutic effect of (-)deprenyl in age-related neurological diseases. Med. Res. Rev. 12 (1992) 505-524.

 

Chapter 4

[83] J. Knoll, I. Miklya, B. Knoll, Stimulation of the catecholaminergic and serotoninergic neurons in the rat brain by R- (-) -1-(benzofuran-2-yl)-2-propylaminopentane, (-)-BPAP, Life Sci. 71 (2002) 2137-2144.

[84] J. Knoll, I. Miklya, Enhanced catecholaminergic and serotoninergic activity in rat brain from weaning to sexual maturity. Rationale for prophylactic (-)deprenyl (selegiline) medication, Life Sci. 56 (1995) 611-620.

[85] J. Knoll, Antiaging compounds: (-)Deprenyl (Selegiline) and (-)1-(benzofuran-2-yl)-2-propylaminopentane, (-)BPAP, a selective highly potent enhancer of the impulse propagation mediated release of catecholamines and serotonin in the brain, CNS Drug Rev. 7 (2001) 317-345.

[86] J. Knoll, Enhancer regulation/endogenous and synthetic enhancer compounds:
A neurochemical concept of the innate and acquired drives, Neurochem. Res. 28 (2003) 1187-1209.

[87] J. Knoll, (-)Deprenyl-medication: A strategy to modulate the age-related decline of the striatal dopaminergic system, J. Am. Ger. Soc. 40 (1992) 839-847.

[88] D. Scherman, P. Jaudon, J. Henry, Characterization of the monoamine transporter of chromaffin granules by binding of [3H]dihidrotetrabenazine, Proc. Natl. Acad. Sci. I.S.A. 80 (1983) 584-588.

[89] J. Glowinski, L.L. Iversen, 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 (1966) 655-669.

[90] L.G. Harsing Jr., H. Sershen, A. Lajtha, Dopamine efflux after chronic nicotine: evidence for autoreceptor desensitization, J. Neurochem. 59 (1992) 48-54.

[91] D.B. Horton, J.B. Nickell, G. Zheng, P.A. Crooks, L.P. Dwoskin, GZ-793A, a lobelane analog, interacts with the vesicular monoamine transporter-2 to inhibit the effect of methamphetamine, J. Neurochem.  127 (2013) 177-186.

[92] J.S. Partilla, A.G. Dempsey, A.S. Nagpal, B.E. Blough, M.H. Baumann, R.B. Rothmann, Interaction of amphetamines and related compounds at the vesicular monoamine transporter, J. Pharmacol. Exp. Ther. 319 (2006) 237-246.

[93] J. Knoll, T.T. Yen, I. Miklya, Sexually low performing male rats dies earlier than their high performing peers and (-)deprenyl treatment eliminates this difference,
Life Sci. 54 (1994) 1047-1057.

[94] J. Knoll, J. Dalló, T.T. Yen, Striatal dopamine, sexual activity and lifespan. Longevity of rats treated with (-)deprenyl, Life Sci. 45 (1989) 525-531.

[95] J. Knoll, I. Miklya, B. Knoll, J. Dalló, Sexual hormones terminate in the rat the significantly enhanced catecholaminergic/serotoninergic tone in the brain characteristic to the post-weaning period, Life Sci. 67 (2000) 765-773.

[96] W. Birkmayer, J. Knoll, P. Riederer, M.B.H. Youdim, V. Hars, V. Marton, Increased life expectancy resulting from addition of L-deprenyl to Madopar treatment in Parkinson's disease: a longterm study, J. Neural Transm. 64 (1985) 113-127.

[97] M. Marinelli, C.N. Rudick, X.T. Hu, F.J. White, Excitability of dopamine neurons: modulation and physiological consequences, CNS Neurol. Dis. Drug Targets 5 (2006) 79-97.

 

Chapter 6

[98] J. Knoll, The pharmacological basis of the beneficial effect of (-)deprenyl (selegiline) in Parkinson's and Alzheimer’s diseases, J. Neural Transm. Suppl 40 (1993) 69-91.

[99] M.W. Milgram, R.J. Racine, P. Nellis, A. Mendonca, G.O. Ivy, Maintenance on L-(-)deprenyl prolongs life in aged male rats, Life Sci. 47 (1990) 415-420.

[100] K. Kitani, S. Kanai, Y. Sato, M.Ohta, G.O. Ivy, M.C. Carrillo, Chronic treatment of (-)deprenyl prolongs the life span of male Fischer 344 rats. Further evidence, Life Sci. 52 (1993) 281-288.

[101] J. Dalló, L. Köles, Longevity treatment with (-)-deprenyl in female rats: effect on copulatory activity and lifespan, Acta Physiol. Hung. 84 (1996) 277-278.

[102] P.C. Bickford, S.J. Adams, P. Boyson, P. Curella, A. Gerhardt, C. Heron, et al., Long-term treatment of male F344 rats with deprenyl: assessment of effects on longevity, behavior, and brain function, Neurobiol. Aging 3 (1997) 309-318.

[103] H.J. Freisleben, F. Lehr, J. Fuchs, Lifespan of immunosuppressed NMRI-mice is increased by (-)-deprenyl, J. Neural Transm. Suppl. 41 (1994) 231-236.

[104] J.R. Archer, D.E. Harrison, L-Deprenyl treatment in aged mice slightly increases life spans, and greatly reduces fecundity by aged males, J. Gerontol. Ser. A – Biol. Sci. Med. 51 (1996) B448-453.

[105] S. Stoll, U. Hafner, B. Kranzlin, W.E. Muller, Chronic treatment of Syrian hamsters with low-dose selegiline increases life span in females but not males, Neurobiol. Aging 18 (1997) 205-211.

[106] W.W. Ruehl, T.L. Entriken, B.A. Muggenburg, D.S. Bruyette, W.C. Griffith, F.F. Hahn, Treatment with L-deprenyl prolongs life in elderly dogs, Life Sci. 61 (1997) 1037-1044

[107] R.G. Jordens, M.D. Berry, C. Gillott, A.A. Boulton, Prolongation of life in an experimental model of aging in Drosophila Melanogaster, Neurochem. Res. 24 (1999) 227-233.

[108] K. Kitani, C. Minami, K. Isobe, K. Maehara, S. Kanai, G.O. Ivy, M.C. Carrillo, Why (-)deprenyl prolongs survivals of experimental animals: Increase of anti-oxidant enzymes in brain and other body tissues as well as mobilization of various humoral factors may lead to systemic anti-aging effects, Mech. Ageing Dev. 123 (2002) 1087-1100.

[109] K. Kitani, S. Kanai, K. Miyasaka, M.C. Carrillo, G.O. Ivy, Dose-dependency of life span prolobgation of F344/DuCrj rats injected with (-)-deprenyl, Biogerontol. 6 (2005) 297-302

[110] D. Bovet, F. Bovet-Nitti, A. Oliverio, Effects of nicotine on avoidance conditioning of inbred strains of mice, Psychopharmacol. 10 (1966) 1-5.

[111] W. Schreiber, J.C. Krieg, T. Eichhorn, Reversal of tetrabenazine induced depression by selective noradrenaline (norepinephrine) reuptake inhibition, J. Neurol. Neurosurg. Psych.  67 (1999) 550.

 

Chapter 7

[112] A. Samuele, A. Mangiagalli, M. Armentero, R. Fancellu, E. Bazzini, M. Vairetti, et al., Oxidative stress and pro-apoptotic conditions in a rodent model of Wilson’s disease, Biochim. Biophys. Acta 1741 (2005) 325-330.

 

Chapter 9

[113] G. Zsilla, J. Knoll, The action of (-)deprenyl on monoamine turnover rate in rat brain, Advances Biochemical Psychopharmacology 31 (1982) 211-217, (Typicalé and Atypical Antidepressants: Molecular Mechanisms. Eds.: E. Costa, G. Racagni).

[114] G. Zsilla, A.M. Szekely, J. Knoll, Influence of neurotransmitter rate and receptor density by repeated low doses of (-)-deprenyl, In: Modulation of Central and Peripheral Transmitter Function. Eds.: G. Biggio, P.F. Spano, G. Toffano, G.L. Gessa, Liviana Press Padiva, (1986) pp. 443-446.

[115] C. Martin, Sexual activity in the aging male, In: J. Money, H. Musaph (Eds), Handbook of sexology, Elsevier, Amsterdam, (1977) pp. 813-824.

[116] J. Knoll, The pharmacology of selegiline /(-)deprenyl/,  Acta Neurol. Scand. 126 (1989) 83-91.

[117] J. Knoll, Nigrostriatal dopaminergic activity, deprenyl treatment, and longevity, Adv. Neurol. 53 (1990) 425-429.

[118] J. Knoll, The pharmacological basis of the beneficial effect of (-)deprenyl (selegiline) in Parkinson's and Alzheimer's diseases, J. Neural Transm. Suppl 40 (1993) 69-91.

[119] J. Knoll, The pharmacological basis of the beneficial effect of (-)deprenyl (selegiline) in Parkinson's and Alzheimer's diseases, J. Neural Transm. Suppl 40 (1993) 69-91.

[120] T.T. Yen, J. Dallo, J. Knoll, The aphrodisiac effect of low doses of (-)deprenyl in male rats, Pol. J. Pharmacol. Pharm. 34 (1982) 303-308.

 

Chapter 10

[121] J. Knoll, K. Baghy, S. Eckhardt, P. Ferdinandy, M. Garami, L.G.Jr. Harsing, P. Hauser, Z. Mervai, T.  Pocza, Z. Schaff, D. Schuler, I. Miklya, A longevity study with enhancer substances (Selegiline, BPAP) detected an unknown tumor-manifestation-suppressing regulation in rat brain, Life Sci. 182 (2017) 57-64.

[122] P.F. Jacobsen, D.J. Jenkyn, J.M. Papdimitriou, Establishment of a human medulloblastoma cell line and its heterotransplantation into nude mice, J. Neuropathol. Exp. Neurol. 44 (1985) 472-85. DOI:10.1097/00005072-198509000-00003

[123] G.E. Keles, M.S. Berger, J. Srinivasan, D.D. Kolstoe, M.S. Bobola, J.R. Silber, Establishment and characterization of four human medulloblastoma cell lines, Oncol. Res. 7 (1995) 493-503.

 

July 4, 2019