Therapeutic applications of selective and non-selective inhibitors of monoamine oxidase A and B that do not cause significant tyramine potentiation
Identifieur interne : 000E41 ( PascalFrancis/Corpus ); précédent : 000E40; suivant : 000E42Therapeutic applications of selective and non-selective inhibitors of monoamine oxidase A and B that do not cause significant tyramine potentiation
Auteurs : Moussa B. H. Youdim ; Marta WeinstockSource :
- Neurotoxicology : (Park Forest South) [ 0161-813X ] ; 2004.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
The major side effect with the use of first generation of non selective monoamine oxidase (MAO) inhibitors as neuropsychiatric drugs was what became known as the "cheese reaction". Namely, potentiation of sympathomimetic activity of ingested tyramine present in cheese and other food stuff, resulting from its ability to release noradrenaline, when prevented from metabolism by MAO. The identification of two forms of MAO, termed types A and B and their selective irreversible inhibitors resolved some of this problems. However irreversible MAO-A inhibitors continue to induce a cheese reaction, whereas MAO-B inhibitors at their selective dosage did not and led to introduction ofL-deprenyl (selegiline) as an anti-Parkinson drug, since dopamine is equally well metabolized by both enzyme forms. The cheese reaction is a consequence of inhibition of MAO-A, the enzyme responsible for metabolism of noradreanline and serotonin, located in peripheral adrenergic neurons. The consequence of these findings were the development of reversible MAO-A inhibitors (RIMA), moclobemide and brofaromin, as antidepressants and possible anti-Parkinson activity, with limited tyramine potentiation, since the amine can displace the inhibitor from its binding site on the enzyme. It has always been deemed a greater pharmacological advantage to inhibit both forms of the enzymes to get the full functional activities of the amine neurotransmitters, and without inducing a "cheese reaction". This was not possible until recently, with the development of the novel cholinesterase-brain selective MAO-AB inhibitor, TV3326 (N-propargyl-(3R)-aminoindan-5-yl-ethyl methylcarbamte hemitartate), a carbamte derivative of the irreversible MAO-B inhibitor anti-Parkinson drug, rasagiline. This drug is a brain selective MAO-A and B inhibitor, with little inhibition of liver and small intestine enzymes. Pharmacologically it has limited tyramine potentiation, very similar to moclobemide and being a MAO-AB inhibitor it has the antidepressant, anti-Parkinson and anti-Alzheimer activities in the respective models used to develop such drugs.
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Format Inist (serveur)
NO : | PASCAL 04-0194375 INIST |
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ET : | Therapeutic applications of selective and non-selective inhibitors of monoamine oxidase A and B that do not cause significant tyramine potentiation |
AU : | YOUDIM (Moussa B. H.); WEINSTOCK (Marta); NICOTRA (A.); PARVEZ (S. H.); GLOVER (V.); SANDLER (M.); PARVEZ (S.); MINAMI (M.) |
AF : | Department of Pharmacology, Bruce Rappaport Faculty of Medicine-Technion, Eve Topf and National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases Research, Efron St, P.O. Box 9697/Haifa 31096/Israël (1 aut.); Department of Pharmacology, Hebrew University Hadassah Medical Center/Jerusalem/Israël (2 aut.); Dept. Animal and Human Biology, University of Rome I, Viale dell'Università 32/00198 Rome/Italie (1 aut.); Institut Alfred Fressard of Neuroscience, Bât5 Parc Chateau, CNRS/91190 Gif sur Yvette/France (2 aut., 5 aut.); Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, Du Cane Road/London, W12 ONN/Royaume-Uni (3 aut., 4 aut.); The Research Institute of Personalized Health, Health Sciences University of Hokkaido/061-0293 Ishikari-Tobetsu/Japon (6 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Neurotoxicology : (Park Forest South); ISSN 0161-813X; Etats-Unis; Da. 2004; Vol. 25; No. 1-2; Pp. 243-250; Bibl. 1 p.1/4 |
LA : | Anglais |
EA : | The major side effect with the use of first generation of non selective monoamine oxidase (MAO) inhibitors as neuropsychiatric drugs was what became known as the "cheese reaction". Namely, potentiation of sympathomimetic activity of ingested tyramine present in cheese and other food stuff, resulting from its ability to release noradrenaline, when prevented from metabolism by MAO. The identification of two forms of MAO, termed types A and B and their selective irreversible inhibitors resolved some of this problems. However irreversible MAO-A inhibitors continue to induce a cheese reaction, whereas MAO-B inhibitors at their selective dosage did not and led to introduction ofL-deprenyl (selegiline) as an anti-Parkinson drug, since dopamine is equally well metabolized by both enzyme forms. The cheese reaction is a consequence of inhibition of MAO-A, the enzyme responsible for metabolism of noradreanline and serotonin, located in peripheral adrenergic neurons. The consequence of these findings were the development of reversible MAO-A inhibitors (RIMA), moclobemide and brofaromin, as antidepressants and possible anti-Parkinson activity, with limited tyramine potentiation, since the amine can displace the inhibitor from its binding site on the enzyme. It has always been deemed a greater pharmacological advantage to inhibit both forms of the enzymes to get the full functional activities of the amine neurotransmitters, and without inducing a "cheese reaction". This was not possible until recently, with the development of the novel cholinesterase-brain selective MAO-AB inhibitor, TV3326 (N-propargyl-(3R)-aminoindan-5-yl-ethyl methylcarbamte hemitartate), a carbamte derivative of the irreversible MAO-B inhibitor anti-Parkinson drug, rasagiline. This drug is a brain selective MAO-A and B inhibitor, with little inhibition of liver and small intestine enzymes. Pharmacologically it has limited tyramine potentiation, very similar to moclobemide and being a MAO-AB inhibitor it has the antidepressant, anti-Parkinson and anti-Alzheimer activities in the respective models used to develop such drugs. |
CC : | 002A25; 002B03; 002B17 |
FD : | Traitement; Sympathomimétique; Application; Tyramine; Potentialisation; Neurologie; Toxicologie; Inhibiteur monoamine oxidase A |
ED : | Treatment; Sympathomimetic; Application; Tyramine; Potentiation; Neurology; Toxicology |
SD : | Tratamiento; Simpaticomimético; Aplicación; Potencialización; Neurología; Toxicología |
LO : | INIST-18397.354000119285470250 |
ID : | 04-0194375 |
Links to Exploration step
Pascal:04-0194375Le document en format XML
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<front><div type="abstract" xml:lang="en">The major side effect with the use of first generation of non selective monoamine oxidase (MAO) inhibitors as neuropsychiatric drugs was what became known as the "cheese reaction". Namely, potentiation of sympathomimetic activity of ingested tyramine present in cheese and other food stuff, resulting from its ability to release noradrenaline, when prevented from metabolism by MAO. The identification of two forms of MAO, termed types A and B and their selective irreversible inhibitors resolved some of this problems. However irreversible MAO-A inhibitors continue to induce a cheese reaction, whereas MAO-B inhibitors at their selective dosage did not and led to introduction ofL-deprenyl (selegiline) as an anti-Parkinson drug, since dopamine is equally well metabolized by both enzyme forms. The cheese reaction is a consequence of inhibition of MAO-A, the enzyme responsible for metabolism of noradreanline and serotonin, located in peripheral adrenergic neurons. The consequence of these findings were the development of reversible MAO-A inhibitors (RIMA), moclobemide and brofaromin, as antidepressants and possible anti-Parkinson activity, with limited tyramine potentiation, since the amine can displace the inhibitor from its binding site on the enzyme. It has always been deemed a greater pharmacological advantage to inhibit both forms of the enzymes to get the full functional activities of the amine neurotransmitters, and without inducing a "cheese reaction". This was not possible until recently, with the development of the novel cholinesterase-brain selective MAO-AB inhibitor, TV3326 (N-propargyl-(3R)-aminoindan-5-yl-ethyl methylcarbamte hemitartate), a carbamte derivative of the irreversible MAO-B inhibitor anti-Parkinson drug, rasagiline. This drug is a brain selective MAO-A and B inhibitor, with little inhibition of liver and small intestine enzymes. Pharmacologically it has limited tyramine potentiation, very similar to moclobemide and being a MAO-AB inhibitor it has the antidepressant, anti-Parkinson and anti-Alzheimer activities in the respective models used to develop such drugs.</div>
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<ET>Therapeutic applications of selective and non-selective inhibitors of monoamine oxidase A and B that do not cause significant tyramine potentiation</ET>
<AU>YOUDIM (Moussa B. H.); WEINSTOCK (Marta); NICOTRA (A.); PARVEZ (S. H.); GLOVER (V.); SANDLER (M.); PARVEZ (S.); MINAMI (M.)</AU>
<AF>Department of Pharmacology, Bruce Rappaport Faculty of Medicine-Technion, Eve Topf and National Parkinson Foundation Centers of Excellence for Neurodegenerative Diseases Research, Efron St, P.O. Box 9697/Haifa 31096/Israël (1 aut.); Department of Pharmacology, Hebrew University Hadassah Medical Center/Jerusalem/Israël (2 aut.); Dept. Animal and Human Biology, University of Rome I, Viale dell'Università 32/00198 Rome/Italie (1 aut.); Institut Alfred Fressard of Neuroscience, Bât5 Parc Chateau, CNRS/91190 Gif sur Yvette/France (2 aut., 5 aut.); Institute of Reproductive and Developmental Biology, Imperial College London, Hammersmith Campus, Du Cane Road/London, W12 ONN/Royaume-Uni (3 aut., 4 aut.); The Research Institute of Personalized Health, Health Sciences University of Hokkaido/061-0293 Ishikari-Tobetsu/Japon (6 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
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<EA>The major side effect with the use of first generation of non selective monoamine oxidase (MAO) inhibitors as neuropsychiatric drugs was what became known as the "cheese reaction". Namely, potentiation of sympathomimetic activity of ingested tyramine present in cheese and other food stuff, resulting from its ability to release noradrenaline, when prevented from metabolism by MAO. The identification of two forms of MAO, termed types A and B and their selective irreversible inhibitors resolved some of this problems. However irreversible MAO-A inhibitors continue to induce a cheese reaction, whereas MAO-B inhibitors at their selective dosage did not and led to introduction ofL-deprenyl (selegiline) as an anti-Parkinson drug, since dopamine is equally well metabolized by both enzyme forms. The cheese reaction is a consequence of inhibition of MAO-A, the enzyme responsible for metabolism of noradreanline and serotonin, located in peripheral adrenergic neurons. The consequence of these findings were the development of reversible MAO-A inhibitors (RIMA), moclobemide and brofaromin, as antidepressants and possible anti-Parkinson activity, with limited tyramine potentiation, since the amine can displace the inhibitor from its binding site on the enzyme. It has always been deemed a greater pharmacological advantage to inhibit both forms of the enzymes to get the full functional activities of the amine neurotransmitters, and without inducing a "cheese reaction". This was not possible until recently, with the development of the novel cholinesterase-brain selective MAO-AB inhibitor, TV3326 (N-propargyl-(3R)-aminoindan-5-yl-ethyl methylcarbamte hemitartate), a carbamte derivative of the irreversible MAO-B inhibitor anti-Parkinson drug, rasagiline. This drug is a brain selective MAO-A and B inhibitor, with little inhibition of liver and small intestine enzymes. Pharmacologically it has limited tyramine potentiation, very similar to moclobemide and being a MAO-AB inhibitor it has the antidepressant, anti-Parkinson and anti-Alzheimer activities in the respective models used to develop such drugs.</EA>
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