The pathogenesis of cell death in Parkinson's disease – 2007
Identifieur interne : 002B32 ( Main/Exploration ); précédent : 002B31; suivant : 002B33The pathogenesis of cell death in Parkinson's disease – 2007
Auteurs : C. Warren Olanow [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2007.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
- Cell Death, Cell death, Disease Progression, Dopamine (metabolism), Familial disease, Humans, Lewy Bodies (pathology), Multicatalytic endopeptidase complex, Nerve Degeneration (metabolism), Nerve Degeneration (physiopathology), Nervous system diseases, Oxidative Stress (physiology), Oxidative stress, Oxygen (metabolism), Parkinson Disease (genetics), Parkinson Disease (metabolism), Parkinson Disease (physiopathology), Parkinson disease, Parkinson's disease, Pathogenesis, Point Mutation (genetics), Proteasome Endopeptidase Complex (physiology), Protein-Serine-Threonine Kinases (genetics), Signal Transduction (physiology), Ubiquitin, Ubiquitin (physiology), alpha-Synuclein (metabolism), familial Parkinson's disease, oxidative stress, pathogenesis, ubiquitin‐proteasome system, α‐synuclein.
- MESH :
- chemical , genetics : Protein-Serine-Threonine Kinases.
- chemical , metabolism : Dopamine, Oxygen, alpha-Synuclein.
- genetics : Parkinson Disease, Point Mutation.
- metabolism : Nerve Degeneration, Parkinson Disease.
- pathology : Lewy Bodies.
- physiology : Oxidative Stress, Proteasome Endopeptidase Complex, Signal Transduction, Ubiquitin.
- physiopathology : Nerve Degeneration, Parkinson Disease.
- Cell Death, Disease Progression, Humans.
Abstract
A number of factors have been implicated in the pathogenesis of cell death in Parkinson's disease (PD). These include oxidative stress, mitochondrial dysfunction, inflammation, excitotoxicity, and apoptosis. While the precise pathogenic mechanism leading to neurodegeneration in PD is not known, there is considerable evidence suggesting that cell death occurs by way of a signal‐mediated apoptotic process. PD is also characterized by intracellular proteinaceous inclusions or Lewy bodies. Proteolytic stress arises as a consequence of the excessive production of misfolded proteins, which exceed the capacity of the ubiquitin‐proteasome system to degrade them. Recent genetic and laboratory studies support the possible relevance of proteolytic stress to both familial and sporadic forms of PD. Postmortem studies have shown that in the SNc of sporadic PD patients there are reduced levels of the alpha subunit of the 20S proteasome and reduced proteolytic enzyme activities. A determination as to the precise cause of cell death in PD, and the identification of specific targets for the development of drugs that might modify disease progression is one of the most critical goals in PD research. It is anticipated that over the next few years there will be a flurry of scientific activity examining the mechanism of cell death and putative neuroprotective interventions. © 2007 Movement Disorder Society
Url:
DOI: 10.1002/mds.21675
Affiliations:
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Le document en format XML
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Warren" last="Olanow">C. Warren Olanow</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Mount Sinai School of Medicine, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neuroscience, Mount Sinai School of Medicine, New York, New York</wicri:regionArea><placeName><region type="state">État de New York</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2007">2007</date><biblScope unit="vol">22</biblScope><biblScope unit="issue">S17</biblScope><biblScope unit="supplement">S17</biblScope><biblScope unit="page" from="S335">S335</biblScope><biblScope unit="page" to="S342">S342</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">BA8CDDB6F69253654F634021ECA32F845F75BF70</idno><idno type="DOI">10.1002/mds.21675</idno><idno type="ArticleID">MDS21675</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell Death</term><term>Cell death</term><term>Disease Progression</term><term>Dopamine (metabolism)</term><term>Familial disease</term><term>Humans</term><term>Lewy Bodies (pathology)</term><term>Multicatalytic endopeptidase complex</term><term>Nerve Degeneration (metabolism)</term><term>Nerve Degeneration (physiopathology)</term><term>Nervous system diseases</term><term>Oxidative Stress (physiology)</term><term>Oxidative stress</term><term>Oxygen (metabolism)</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Pathogenesis</term><term>Point Mutation (genetics)</term><term>Proteasome Endopeptidase Complex (physiology)</term><term>Protein-Serine-Threonine Kinases (genetics)</term><term>Signal Transduction (physiology)</term><term>Ubiquitin</term><term>Ubiquitin (physiology)</term><term>alpha-Synuclein (metabolism)</term><term>familial Parkinson's disease</term><term>oxidative stress</term><term>pathogenesis</term><term>ubiquitin‐proteasome system</term><term>α‐synuclein</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Protein-Serine-Threonine Kinases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dopamine</term><term>Oxygen</term><term>alpha-Synuclein</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term><term>Point Mutation</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lewy Bodies</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Oxidative Stress</term><term>Proteasome Endopeptidase Complex</term><term>Signal Transduction</term><term>Ubiquitin</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Nerve Degeneration</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Cell Death</term><term>Disease Progression</term><term>Humans</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term><term>Maladie familiale</term><term>Mort cellulaire</term><term>Multicatalytic endopeptidase complex</term><term>Pathogénie</term><term>Pathologie du système nerveux</term><term>Stress oxydatif</term><term>Ubiquitine</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A number of factors have been implicated in the pathogenesis of cell death in Parkinson's disease (PD). These include oxidative stress, mitochondrial dysfunction, inflammation, excitotoxicity, and apoptosis. While the precise pathogenic mechanism leading to neurodegeneration in PD is not known, there is considerable evidence suggesting that cell death occurs by way of a signal‐mediated apoptotic process. PD is also characterized by intracellular proteinaceous inclusions or Lewy bodies. Proteolytic stress arises as a consequence of the excessive production of misfolded proteins, which exceed the capacity of the ubiquitin‐proteasome system to degrade them. Recent genetic and laboratory studies support the possible relevance of proteolytic stress to both familial and sporadic forms of PD. Postmortem studies have shown that in the SNc of sporadic PD patients there are reduced levels of the alpha subunit of the 20S proteasome and reduced proteolytic enzyme activities. A determination as to the precise cause of cell death in PD, and the identification of specific targets for the development of drugs that might modify disease progression is one of the most critical goals in PD research. It is anticipated that over the next few years there will be a flurry of scientific activity examining the mechanism of cell death and putative neuroprotective interventions. © 2007 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>État de New York</li></region></list><tree><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="Olanow, C Warren" sort="Olanow, C Warren" uniqKey="Olanow C" first="C. Warren" last="Olanow">C. Warren Olanow</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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