Slowing of neurodegeneration in Parkinson's disease and Huntington's disease: future therapeutic perspectives.
Identifieur interne : 000218 ( France/Analysis ); précédent : 000217; suivant : 000219Slowing of neurodegeneration in Parkinson's disease and Huntington's disease: future therapeutic perspectives.
Auteurs : Anthony H V. Schapira [Royaume-Uni] ; C Warren Olanow [États-Unis] ; J Timothy Greenamyre [États-Unis] ; Erwan Bezard [France]Source :
- Lancet (London, England) [ 1474-547X ] ; 2014.
Descripteurs français
- KwdFr :
- Apoptose (), Humains, Maladie de Huntington (métabolisme), Maladie de Huntington (traitement médicamenteux), Maladie de Parkinson (métabolisme), Maladie de Parkinson (traitement médicamenteux), Mitochondries (), Mitochondries (métabolisme), Neuroprotecteurs (pharmacologie), Neuroprotecteurs (usage thérapeutique), Protein kinases (), Protein kinases (métabolisme), Récepteur facteur croissance (), Récepteur facteur croissance (métabolisme), Stress oxydatif (), Transduction du signal ().
- MESH :
- métabolisme : Maladie de Huntington, Maladie de Parkinson, Mitochondries, Protein kinases, Récepteur facteur croissance.
- pharmacologie : Neuroprotecteurs.
- traitement médicamenteux : Maladie de Huntington, Maladie de Parkinson.
- usage thérapeutique : Neuroprotecteurs.
- Apoptose, Humains, Mitochondries, Protein kinases, Récepteur facteur croissance, Stress oxydatif, Transduction du signal.
English descriptors
- KwdEn :
- Apoptosis (drug effects), Humans, Huntington Disease (drug therapy), Huntington Disease (metabolism), Mitochondria (drug effects), Mitochondria (metabolism), Neuroprotective Agents (pharmacology), Neuroprotective Agents (therapeutic use), Oxidative Stress (drug effects), Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Protein Kinases (drug effects), Protein Kinases (metabolism), Receptors, Growth Factor (drug effects), Receptors, Growth Factor (metabolism), Signal Transduction (drug effects).
- MESH :
- chemical , drug effects : Protein Kinases, Receptors, Growth Factor.
- chemical , metabolism : Protein Kinases, Receptors, Growth Factor.
- chemical , pharmacology : Neuroprotective Agents.
- drug effects : Apoptosis, Mitochondria, Oxidative Stress, Signal Transduction.
- drug therapy : Huntington Disease, Parkinson Disease.
- metabolism : Huntington Disease, Mitochondria, Parkinson Disease.
- chemical , therapeutic use : Neuroprotective Agents.
- Humans.
Abstract
Several important advances have been made in our understanding of the pathways that lead to cell dysfunction and death in Parkinson's disease and Huntington's disease. These advances have been informed by both direct analysis of the post-mortem brain and by study of the biological consequences of the genetic causes of these diseases. Some of the pathways that have been implicated so far include mitochondrial dysfunction, oxidative stress, kinase pathways, calcium dysregulation, inflammation, protein handling, and prion-like processes. Intriguingly, these pathways seem to be important in the pathogenesis of both diseases and have led to the identification of molecular targets for candidate interventions designed to slow or reverse their course. We review some recent advances that underlie putative therapies for neuroprotection in Parkinson's disease and Huntington's disease, and potential targets that might be exploited in the future. Although we will need to overcome important hurdles, especially in terms of clinical trial design, we propose several target pathways that merit further study. In Parkinson's disease, these targets include agents that might improve mitochondrial function or increase degradation of defective mitochondria, kinase inhibitors, calcium channel blockers, and approaches that interfere with the misfolding, templating, and transmission of α-synuclein. In Huntington's disease, strategies might also be directed at mitochondrial bioenergetics and turnover, the prevention of protein dysregulation, disruption of the interaction between huntingtin and p53 or huntingtin-interacting protein 1 to reduce apoptosis, and interference with expression of mutant huntingtin at both the nucleic acid and protein levels.
DOI: 10.1016/S0140-6736(14)61010-2
PubMed: 24954676
Affiliations:
- France, Royaume-Uni, États-Unis
- Angleterre, Aquitaine, Grand Londres, Nouvelle-Aquitaine, Pennsylvanie, État de New York
- Bordeaux, Londres, Pittsburgh
- Université de Bordeaux, Université de Pittsburgh
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pubmed:24954676Le document en format XML
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Schapira</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Neurosciences, UCL Institute of Neurology, London, UK. Electronic address: a.schapira@ucl.ac.uk.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Clinical Neurosciences, UCL Institute of Neurology, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Olanow, C Warren" sort="Olanow, C Warren" uniqKey="Olanow C" first="C Warren" last="Olanow">C Warren Olanow</name><affiliation wicri:level="2"><nlm:affiliation>Departments of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, NY, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Departments of Neurology and Neuroscience, Mount Sinai School of Medicine, New York, NY</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Greenamyre, J Timothy" sort="Greenamyre, J Timothy" uniqKey="Greenamyre J" first="J Timothy" last="Greenamyre">J Timothy Greenamyre</name><affiliation wicri:level="4"><nlm:affiliation>Pittsburgh Institute for Neurodegenerative Diseases, University of Pittsburgh, Pittsburgh, PA 15260, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Pittsburgh Institute for Neurodegenerative Diseases, University of Pittsburgh, Pittsburgh, PA 15260</wicri:regionArea><placeName><region type="state">Pennsylvanie</region><settlement type="city">Pittsburgh</settlement></placeName><orgName type="university">Université de Pittsburgh</orgName></affiliation></author><author><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name><affiliation wicri:level="4"><nlm:affiliation>Université de Bordeaux, Institut des Maladies Neurodégénératives, 33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, 33000 Bordeaux, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>Université de Bordeaux, Institut des Maladies Neurodégénératives, 33000 Bordeaux, France; CNRS, Institut des Maladies Neurodégénératives, 33000 Bordeaux</wicri:regionArea><wicri:noRegion>33000 Bordeaux</wicri:noRegion><orgName type="university">Université de Bordeaux</orgName><placeName><settlement type="city">Bordeaux</settlement><region type="region" nuts="2">Nouvelle-Aquitaine</region><region type="old region" nuts="2">Aquitaine</region></placeName></affiliation></author></analytic><series><title level="j">Lancet (London, England)</title><idno type="eISSN">1474-547X</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis (drug effects)</term><term>Humans</term><term>Huntington Disease (drug therapy)</term><term>Huntington Disease (metabolism)</term><term>Mitochondria (drug effects)</term><term>Mitochondria (metabolism)</term><term>Neuroprotective Agents (pharmacology)</term><term>Neuroprotective Agents (therapeutic use)</term><term>Oxidative Stress (drug effects)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (metabolism)</term><term>Protein Kinases (drug effects)</term><term>Protein Kinases (metabolism)</term><term>Receptors, Growth Factor (drug effects)</term><term>Receptors, Growth Factor (metabolism)</term><term>Signal Transduction (drug effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Apoptose ()</term><term>Humains</term><term>Maladie de Huntington (métabolisme)</term><term>Maladie de Huntington (traitement médicamenteux)</term><term>Maladie de Parkinson (métabolisme)</term><term>Maladie de Parkinson (traitement médicamenteux)</term><term>Mitochondries ()</term><term>Mitochondries (métabolisme)</term><term>Neuroprotecteurs (pharmacologie)</term><term>Neuroprotecteurs (usage thérapeutique)</term><term>Protein kinases ()</term><term>Protein kinases (métabolisme)</term><term>Récepteur facteur croissance ()</term><term>Récepteur facteur croissance (métabolisme)</term><term>Stress oxydatif ()</term><term>Transduction du signal ()</term></keywords><keywords scheme="MESH" type="chemical" qualifier="drug effects" xml:lang="en"><term>Protein Kinases</term><term>Receptors, Growth Factor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Protein Kinases</term><term>Receptors, Growth Factor</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Apoptosis</term><term>Mitochondria</term><term>Oxidative Stress</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Huntington Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Huntington Disease</term><term>Mitochondria</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Maladie de Huntington</term><term>Maladie de Parkinson</term><term>Mitochondries</term><term>Protein kinases</term><term>Récepteur facteur croissance</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Neuroprotecteurs</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Neuroprotective Agents</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Maladie de Huntington</term><term>Maladie de Parkinson</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Neuroprotecteurs</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Humans</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Apoptose</term><term>Humains</term><term>Mitochondries</term><term>Protein kinases</term><term>Récepteur facteur croissance</term><term>Stress oxydatif</term><term>Transduction du signal</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Several important advances have been made in our understanding of the pathways that lead to cell dysfunction and death in Parkinson's disease and Huntington's disease. These advances have been informed by both direct analysis of the post-mortem brain and by study of the biological consequences of the genetic causes of these diseases. Some of the pathways that have been implicated so far include mitochondrial dysfunction, oxidative stress, kinase pathways, calcium dysregulation, inflammation, protein handling, and prion-like processes. Intriguingly, these pathways seem to be important in the pathogenesis of both diseases and have led to the identification of molecular targets for candidate interventions designed to slow or reverse their course. We review some recent advances that underlie putative therapies for neuroprotection in Parkinson's disease and Huntington's disease, and potential targets that might be exploited in the future. Although we will need to overcome important hurdles, especially in terms of clinical trial design, we propose several target pathways that merit further study. In Parkinson's disease, these targets include agents that might improve mitochondrial function or increase degradation of defective mitochondria, kinase inhibitors, calcium channel blockers, and approaches that interfere with the misfolding, templating, and transmission of α-synuclein. In Huntington's disease, strategies might also be directed at mitochondrial bioenergetics and turnover, the prevention of protein dysregulation, disruption of the interaction between huntingtin and p53 or huntingtin-interacting protein 1 to reduce apoptosis, and interference with expression of mutant huntingtin at both the nucleic acid and protein levels.</div></front></TEI><affiliations><list><country><li>France</li><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Aquitaine</li><li>Grand Londres</li><li>Nouvelle-Aquitaine</li><li>Pennsylvanie</li><li>État de New York</li></region><settlement><li>Bordeaux</li><li>Londres</li><li>Pittsburgh</li></settlement><orgName><li>Université de Bordeaux</li><li>Université de Pittsburgh</li></orgName></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Schapira, Anthony H V" sort="Schapira, Anthony H V" uniqKey="Schapira A" first="Anthony H V" last="Schapira">Anthony H V. Schapira</name></region></country><country name="États-Unis"><region name="État de New York"><name sortKey="Olanow, C Warren" sort="Olanow, C Warren" uniqKey="Olanow C" first="C Warren" last="Olanow">C Warren Olanow</name></region><name sortKey="Greenamyre, J Timothy" sort="Greenamyre, J Timothy" uniqKey="Greenamyre J" first="J Timothy" last="Greenamyre">J Timothy Greenamyre</name></country><country name="France"><region name="Nouvelle-Aquitaine"><name sortKey="Bezard, Erwan" sort="Bezard, Erwan" uniqKey="Bezard E" first="Erwan" last="Bezard">Erwan Bezard</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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