Hostname: page-component-78c5997874-v9fdk Total loading time: 0 Render date: 2024-11-10T09:40:29.988Z Has data issue: false hasContentIssue false
  • English
  • Français

New Approaches to the Treatment of Age-Related Brain Disorders

Published online by Cambridge University Press:  18 September 2015

M. Da Prada
M. Da Prada*
Affiliation:
Pharma Research Department, F. Hoffmann-La Roche Ltd., Basel, Switzerland
*
Pharma Research Department, F. Hoffmann-La Roche Ltd., Ch-4002 Basel, Switzerland
Rights & Permissions [Opens in a new window]

Abstract:

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

Two novel reversible enzyme inhibitors involved in monoamine metabolism are described. The novel and reversible inhibitors are the catechol-O-methyl-transferase (COMT) inhibitor, Ro 40-7592 (3,4-dihydroxy-4'-methyl-5-nitrobenzophenone), and the monoamine oxidase type-B (MAO-B) inhibitor, Ro 19-6327 (N-(2-aminoethyl)-5-chloro-2-pyridine carboxamide HC1). These may be of special therapeutic benefit in Parkinson's and Alzheimer's diseases.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 18 , Issue S3 , August 1991 , pp. 384 - 386
Copyright
Copyright © Canadian Neurological Sciences Federation 1991

References

REFERENCES

1.Da Prada, M, Zürcher, G, Kettler, R, et al. New therapeutic strategies in Parkinson's disease: inhibition of MAO-B by Ro 19–6327 and of COMT by Ro 40–7592. Adv Behav Biol 1991; 39: 723–732.CrossRefGoogle Scholar
2.Glover, V, Sandler, M, Owen, F, et al. Dopamine is a monoamine oxidase B substrate in man. Nature 1977; 265: 80–81.CrossRefGoogle ScholarPubMed
3.Birkmayer, W, Riederer, P, Youdim, MBH, et al. Potentiation of antikinetic effect after L-dopa treatment by an inhibitor of MAO-B, L-deprenyl J Neural Transm 1975; 36: 303–323.CrossRefGoogle Scholar
4.Heikkila, RE, Manzino, L, Cabbat, FS, et al. Protection against the dopaminergic neurotoxicity of l-methyl-4-phenyl-l, 2, 5, 6-tetrahydropyridine by monoamine oxidase inhibitors. Nature 1984;311:467–469.CrossRefGoogle Scholar
5.Haefely, WE, Kettler, R, Keller, HH, et al. Ro 19–6327, a reversible and highly selective monoamine oxidase B inhibitor: a novel tool to explore the MAO-B function in humans. Adv Neurol 1990; 53:505–512.Google ScholarPubMed
6.Tanner, CM, Langston, JW. Do environmental toxins cause Parkinson’s disease? A critical review. Neurology 1980; 40 (Suppl3): 17–30.Google Scholar
7., W, Knoll, J, Riederer, P, et al. Increased life expectancy resulting from addition of L-deprenyl to Madopar treatment in Parkinson’s disease: a long-term study. J Neural Transm 1985; 64: 113–127.CrossRefGoogle Scholar
8.Langston, JW. Selegiline as neuroprotective therapy in Parkinson’s disease: concepts and controversies. Neurology 1980; 40 (Suppl 3): 61–66.Google Scholar
9.Tariot, PN, Cohen, RM, Sunderlant, T, et al. L-deprenyl in Alz-heimer’s disease. Arch Gen Psychiatry 1987; 44: 427–433.CrossRefGoogle Scholar
10.Piccinin, GL, Finali, G, Piccinini, M. Neuropsychological effects of L-deprenyl in Alzheimer’s type dementia. Clin Neuropharmacol 1990; 13: 147–163.CrossRefGoogle ScholarPubMed
11.Olanov, CW. Oxidation reactions in Parkinson’s disease. Neurology 1990; 40 (Suppl 3): 32–39.Google Scholar
12.Youdim, MBH. Iron in the brain: implications for Parkinson’s and Alzheimer’s diseases. Mt Sinai J Med (NY) 1988; 55: 97–101.Google ScholarPubMed
13.Da Prada, M, Keller, HH, Pieri, L, et al. The pharmacology of Parkinson’s disease: basic aspects and recent advances. Experientia 1984; 40: 1165–1172.CrossRefGoogle ScholarPubMed
14.Koller, WC, Hubble, JP. Levodopa therapy in Parkinson’s disease. Neurology 1990; 40 (Suppl 3): 40–47.Google ScholarPubMed
15.Cedarbaum, JM. Clinical pharmacokinetics of antiparkinsonian drugs. Clin Pharmacokin 1987; 13: 141–178.CrossRefGoogle Scholar
16. <Madopar> HBS. Europ Neurol 1987; 27 (Suppl 1): 1–138.+HBS.+Europ+Neurol1987;+27+(Suppl+1):+1–138.>Google Scholar
17.Lees, AJ. Madopar HBS (hydrodynamically balanced system) in the treatment of Parkinsos’n disease. Adv Neurol 1990; 53: 475–482.Google ScholarPubMed
18.Zürcher, G, Keller, HH, Kettler, R, et al. Ro 40-7592, a novel, very potent and orally active inhibitor of catechol-O-methyltrans-ferase: a pharmacological study in rats. Adv Neurol 1990; 53: 497–503.Google ScholarPubMed
19.Koller, WC, Giron, LT. Selegiline HC1: selective MAO-type B inhibitor. Neurology 1990; 40 (Suppl 3): 58–60.Google ScholarPubMed
20.Reynolds, GP, Elsworth, JP, Blank, K, et al. Deprenyl is metabolized to methamphetamine and amphetamine in man. Brit J Clin Pharmacol 1978; 6: 542–544.CrossRefGoogle ScholarPubMed
21.Price, GW, Bench, CJ, Cremer, JC, et al. Inhibition of human brain monoamine oxidase B by Ro 19-6327 - in vivo measurement using positron emission tomography. Eur J Pharmacol 1990; 183: 166.CrossRefGoogle Scholar