Molecular pathways involved in the neurotoxicity of 6-OHDA, dopamine and MPTP: contribution to the apoptotic theory in Parkinson's disease
Identifieur interne : 001221 ( Istex/Curation ); précédent : 001220; suivant : 001222Molecular pathways involved in the neurotoxicity of 6-OHDA, dopamine and MPTP: contribution to the apoptotic theory in Parkinson's disease
Auteurs : David Blum [Belgique, France] ; Sakina Torch [France] ; Nathalie Lambeng [France] ; Marie Nissou [France] ; Alim Benabid [France] ; Rémy Sadoul [France] ; Jean Verna [France]Source :
- Progress in Neurobiology [ 0301-0082 ] ; 2001.
English descriptors
- KwdEn :
- 6-OHDA, 6-OHDA, 6-hydroxydopamine, 8OHDG, 8-hydroxy-2′deoxy-guanosine, AIF, apoptosis-inducing factor, Animal models, Apoptosis, BIR, baculovirus IAP-repeat, BRUCE, BIR-repeat-containing ubiquitin conjugating enzyme, CA, catecholamine, CARD, caspase recruitment domain, DA, dopamine, DED, death effector domain, DISC, death-inducing signal complex, Dopamine, FADD, Fas-associated death domain, GSH, gluthation, IAP, inhibitory apoptosis protein, ICE, interleukin-1β converting enzyme, JIP, JNK-interacting proteins, JNK, c-jun N-terminal kinase, JNKK, JNK kinase, MAO, monoamine oxidase, MAO-I, inhibitor of monoamine oxidase, MAP, mitogen-activated protein, MKK, MAP kinase kinase, MPDP+, 1-methyl-phenyl-dihydropyridinium, MPP+, MPP+, 1-methyl-4-phenylpyridinium, MPTP, MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, NA, noradrenaline, NF-κB, nuclear factor-κB, NGF, nerve growth factor, NMDA, N-methyl-d-aspartate, NO, nitric oxide, OXPHOS, oxidative phosphorylation system, PARP, poly-ADP-ribose polymerase, PD, Parkinson's disease, PTP, permeability transition pore, Par-4, prostate apoptosis response-4, Parkinson's disease, ROS, reactive oxygen species, SAPK, stress-activated protein kinase, SNpc, substantia nigra pars compacta, TH, tyrosine hydroxylase, TNFα tumor necrosis factor α, TUNEL, (TdT)-mediated dUTP nick-end labeling, VMAT, vesicular monoamine transporters, iNOS, inducible nitric oxide synthase, l-dopa, l-dihydroxyphenylalanine, αKGDH, α-ketoglutarate deshydrogenase.
Abstract
Parkinson's disease (PD) is a neurodegenerative disorder characterized by a preferential loss of the dopaminergic neurons of the substantia nigra pars compacta. Although the etiology of PD is unknown, major biochemical processes such as oxidative stress and mitochondrial inhibition are largely described. However, despite these findings, the actual therapeutics are essentially symptomatical and are not able to block the degenerative process. Recent histological studies performed on brains from PD patients suggest that nigral cell death could be apoptotic. However, since post-mortem studies do not allow precise determination of the sequence of events leading to this apoptotic cell death, the molecular pathways involved in this process have been essentially studied on experimental models reproducing the human disease. These latter are created by using neurotoxic compounds such as 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or dopamine (DA). Extensive study of these models have shown that they mimick, in vitro and in vivo, the histological and/or the biochemical characteristics of PD and thus help to define important cellular actors of cell death presumably critical for the nigral degeneration. This review reports recent data concerning the biochemical and molecular apoptotic mechanisms underlying the experimental models of PD and correlates them to the phenomena occurring in human disease.
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DOI: 10.1016/S0301-0082(01)00003-X
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wicri:rule="url">Belgique</country></affiliation><affiliation wicri:level="1"><mods:affiliation>Unité Mixte INSERM/UJF E0108, Neurodégénérescence et plasticité, CHU Michallon, Pavillon de Neurologie, BP217, 38043 Grenoble Cedex 9, France</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Unité Mixte INSERM/UJF E0108, Neurodégénérescence et plasticité, CHU Michallon, Pavillon de Neurologie, BP217, 38043 Grenoble Cedex 9</wicri:regionArea></affiliation></author><author><name sortKey="Torch, Sakina" sort="Torch, Sakina" uniqKey="Torch S" first="Sakina" last="Torch">Sakina Torch</name><affiliation wicri:level="1"><mods:affiliation>Unité Mixte INSERM/UJF E0108, Neurodégénérescence et plasticité, CHU Michallon, Pavillon de Neurologie, BP217, 38043 Grenoble Cedex 9, France</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Unité Mixte INSERM/UJF E0108, Neurodégénérescence et plasticité, CHU Michallon, Pavillon de Neurologie, BP217, 38043 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Alim Louis" uniqKey="Benabid A" first="Alim" last="Benabid">Alim Benabid</name><affiliation wicri:level="1"><mods:affiliation>INSERM U318, Neurobiologie Préclinique, CHU Michallon, Pav B, BP217, 38043 Grenoble Cedex 9, France</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM U318, Neurobiologie Préclinique, CHU Michallon, Pav B, BP217, 38043 Grenoble Cedex 9</wicri:regionArea></affiliation></author><author><name sortKey="Sadoul, Remy" sort="Sadoul, Remy" uniqKey="Sadoul R" first="Rémy" last="Sadoul">Rémy Sadoul</name><affiliation wicri:level="1"><mods:affiliation>Unité Mixte INSERM/UJF E0108, Neurodégénérescence et plasticité, CHU Michallon, Pavillon de Neurologie, BP217, 38043 Grenoble Cedex 9, France</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Unité Mixte INSERM/UJF E0108, Neurodégénérescence et plasticité, CHU Michallon, Pavillon de Neurologie, BP217, 38043 Grenoble Cedex 9</wicri:regionArea></affiliation></author><author><name sortKey="Verna, Jean Marc" sort="Verna, Jean Marc" uniqKey="Verna J" first="Jean" last="Verna">Jean Verna</name><affiliation wicri:level="1"><mods:affiliation>Unité Mixte INSERM/UJF E0108, Neurodégénérescence et plasticité, CHU Michallon, Pavillon de Neurologie, BP217, 38043 Grenoble Cedex 9, France</mods:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Unité Mixte INSERM/UJF E0108, Neurodégénérescence et plasticité, CHU Michallon, Pavillon de Neurologie, BP217, 38043 Grenoble Cedex 9</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Progress in Neurobiology</title><title level="j" type="abbrev">PRONEU</title><idno type="ISSN">0301-0082</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001">2001</date><biblScope unit="volume">65</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="135">135</biblScope><biblScope unit="page" to="172">172</biblScope></imprint><idno type="ISSN">0301-0082</idno></series><idno type="istex">D45EF552419A01737D9317A747EDAE8180B0CC43</idno><idno type="DOI">10.1016/S0301-0082(01)00003-X</idno><idno type="PII">S0301-0082(01)00003-X</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0301-0082</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>6-OHDA</term><term>6-OHDA, 6-hydroxydopamine</term><term>8OHDG, 8-hydroxy-2′deoxy-guanosine</term><term>AIF, apoptosis-inducing factor</term><term>Animal models</term><term>Apoptosis</term><term>BIR, baculovirus IAP-repeat</term><term>BRUCE, BIR-repeat-containing ubiquitin conjugating enzyme</term><term>CA, catecholamine</term><term>CARD, caspase recruitment domain</term><term>DA, dopamine</term><term>DED, death effector domain</term><term>DISC, death-inducing signal complex</term><term>Dopamine</term><term>FADD, Fas-associated death domain</term><term>GSH, gluthation</term><term>IAP, inhibitory apoptosis protein</term><term>ICE, interleukin-1β converting enzyme</term><term>JIP, JNK-interacting proteins</term><term>JNK, c-jun N-terminal kinase</term><term>JNKK, JNK kinase</term><term>MAO, monoamine oxidase</term><term>MAO-I, inhibitor of monoamine oxidase</term><term>MAP, mitogen-activated protein</term><term>MKK, MAP kinase kinase</term><term>MPDP+, 1-methyl-phenyl-dihydropyridinium</term><term>MPP+</term><term>MPP+, 1-methyl-4-phenylpyridinium</term><term>MPTP</term><term>MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>NA, noradrenaline</term><term>NF-κB, nuclear factor-κB</term><term>NGF, nerve growth factor</term><term>NMDA, N-methyl-d-aspartate</term><term>NO, nitric oxide</term><term>OXPHOS, oxidative phosphorylation system</term><term>PARP, poly-ADP-ribose polymerase</term><term>PD, Parkinson's disease</term><term>PTP, permeability transition pore</term><term>Par-4, prostate apoptosis response-4</term><term>Parkinson's disease</term><term>ROS, reactive oxygen species</term><term>SAPK, stress-activated protein kinase</term><term>SNpc, substantia nigra pars compacta</term><term>TH, tyrosine hydroxylase</term><term>TNFα tumor necrosis factor α</term><term>TUNEL, (TdT)-mediated dUTP nick-end labeling</term><term>VMAT, vesicular monoamine transporters</term><term>iNOS, inducible nitric oxide synthase</term><term>l-dopa, l-dihydroxyphenylalanine</term><term>αKGDH, α-ketoglutarate deshydrogenase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a neurodegenerative disorder characterized by a preferential loss of the dopaminergic neurons of the substantia nigra pars compacta. Although the etiology of PD is unknown, major biochemical processes such as oxidative stress and mitochondrial inhibition are largely described. However, despite these findings, the actual therapeutics are essentially symptomatical and are not able to block the degenerative process. Recent histological studies performed on brains from PD patients suggest that nigral cell death could be apoptotic. However, since post-mortem studies do not allow precise determination of the sequence of events leading to this apoptotic cell death, the molecular pathways involved in this process have been essentially studied on experimental models reproducing the human disease. These latter are created by using neurotoxic compounds such as 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or dopamine (DA). Extensive study of these models have shown that they mimick, in vitro and in vivo, the histological and/or the biochemical characteristics of PD and thus help to define important cellular actors of cell death presumably critical for the nigral degeneration. This review reports recent data concerning the biochemical and molecular apoptotic mechanisms underlying the experimental models of PD and correlates them to the phenomena occurring in human disease.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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