Parkinson's Disease, Proteins, and Prions: Milestones
Identifieur interne : 001A54 ( Main/Merge ); précédent : 001A53; suivant : 001A55Parkinson's Disease, Proteins, and Prions: Milestones
Auteurs : C. Warren Olanow [États-Unis] ; K. Mcnaught [États-Unis]Source :
- Movement disorders [ 0885-3185 ] ; 2011.
Descripteurs français
- Pascal (Inist)
English descriptors
Abstract
Parkinson's disease (PD) is characterized by protein accumulation in the form of Lewy bodies and neurites. It is thus reasonable to consider that alterations in protein handling in the form of increased production, impaired clearance, or both might be central to the etiopathogenesis of the disease. Increasing genetic, laboratory and pathologic evidence has accumulated over the past 25 years supporting this hypothesis. A vicious cycle could develop in which increased protein accumulation from any cause could lead to interference with lysosomal and proteasomal clearance mechanisms causing further protein accumulation. Eventually, protein accumulation could overwhelm the cell's defenses and lead to the formation of toxic oligomers and amyloid-based inclusions such as Lewy bodies, disruption of critical cell processes, and ultimately neurodegeneration. More recent findings of Lewy pathology in implanted embryonic dopamine neurons in PD patients raises the intriguing possibility that PD might be a prion disorder. These concepts suggests new targets and novel candidate therapies that might be neuroprotective for PD.
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Pascal:11-0264654Le document en format XML
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Mcnaught</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>National Tourette Syndrome Association</s1><s2>Bayside, New York</s2><s3>USA</s3><sZ>2 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">État de New York</region></placeName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">11-0264654</idno><date when="2011">2011</date><idno type="stanalyst">PASCAL 11-0264654 INIST</idno><idno type="RBID">Pascal:11-0264654</idno><idno type="wicri:Area/PascalFrancis/Corpus">000574</idno><idno type="wicri:Area/PascalFrancis/Curation">002744</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000464</idno><idno type="wicri:doubleKey">0885-3185:2011:Olanow C:parkinson:s:disease</idno><idno type="wicri:Area/Main/Merge">001A54</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Parkinson's Disease, Proteins, and Prions: Milestones</title><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"><inist:fA14 i1="01"><s1>Department of Neurology and Neuroscience, Mount Sinai School of Medicine</s1><s2>New York, New York</s2><s3>USA</s3><sZ>1 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">État de New York</region></placeName></affiliation></author><author><name sortKey="Mcnaught, K" sort="Mcnaught, K" uniqKey="Mcnaught K" first="K." last="Mcnaught">K. Mcnaught</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>National Tourette Syndrome Association</s1><s2>Bayside, New York</s2><s3>USA</s3><sZ>2 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">État de New York</region></placeName></affiliation></author></analytic><series><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Movement disorders</title><title level="j" type="abbreviated">Mov. disord.</title><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Nervous system diseases</term><term>Parkinson disease</term><term>Prion</term><term>Prion protein</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Protéine PrP</term><term>Prion</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is characterized by protein accumulation in the form of Lewy bodies and neurites. It is thus reasonable to consider that alterations in protein handling in the form of increased production, impaired clearance, or both might be central to the etiopathogenesis of the disease. Increasing genetic, laboratory and pathologic evidence has accumulated over the past 25 years supporting this hypothesis. A vicious cycle could develop in which increased protein accumulation from any cause could lead to interference with lysosomal and proteasomal clearance mechanisms causing further protein accumulation. Eventually, protein accumulation could overwhelm the cell's defenses and lead to the formation of toxic oligomers and amyloid-based inclusions such as Lewy bodies, disruption of critical cell processes, and ultimately neurodegeneration. More recent findings of Lewy pathology in implanted embryonic dopamine neurons in PD patients raises the intriguing possibility that PD might be a prion disorder. These concepts suggests new targets and novel candidate therapies that might be neuroprotective for PD.</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="Mcnaught, K" sort="Mcnaught, K" uniqKey="Mcnaught K" first="K." last="Mcnaught">K. Mcnaught</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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