Modulation of neurodegeneration by molecular chaperones
Identifieur interne : 001480 ( Main/Curation ); précédent : 001479; suivant : 001481Modulation of neurodegeneration by molecular chaperones
Auteurs : Paul J. Muchowski [États-Unis] ; Jennifer L. Wacker [États-Unis]Source :
- Nature Reviews Neuroscience [ 1471-003X ] ; 2005-01.
Abstract
Many neurodegenerative disorders are characterized by conformational changes in proteins that result in misfolding, aggregation and intra- or extra-neuronal accumulation of amyloid fibrils. Molecular chaperones provide a first line of defence against misfolded, aggregation-prone proteins and are among the most potent suppressors of neurodegeneration known for animal models of human disease. Recent studies have investigated the role of molecular chaperones in amyotrophic lateral sclerosis, Alzheimer's disease, Parkinson's disease and polyglutamine diseases. We propose that molecular chaperones are neuroprotective because of their ability to modulate the earliest aberrant protein interactions that trigger pathogenic cascades. A detailed understanding of the molecular basis of chaperone-mediated protection against neurodegeneration might lead to the development of therapies for neurodegenerative disorders that are associated with protein misfolding and aggregation.
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DOI: 10.1038/nrn1587
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Muchowski</name><affiliation wicri:level="1"><mods:affiliation>Department of Pharmacology, University of Washington, Seattle, Washington 98195-7280, USA.</mods:affiliation><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Pharmacology, University of Washington, Seattle, Washington 98195-7280</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>The Center for Neurogenetics and Neurotherapeutics, University of Washington, Seattle, Washington 98195-7280, USA.</mods:affiliation><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>The Center for Neurogenetics and Neurotherapeutics, University of Washington, Seattle, Washington 98195-7280</wicri:regionArea></affiliation><affiliation wicri:level="1"><mods:affiliation>E-mail: mucho@u.washington.edu</mods:affiliation><country wicri:rule="url">États-Unis</country></affiliation></author><author><name sortKey="Wacker, Jennifer L" sort="Wacker, Jennifer L" uniqKey="Wacker J" first="Jennifer L." last="Wacker">Jennifer L. Wacker</name><affiliation wicri:level="1"><mods:affiliation>Department of Pharmacology, University of Washington, Seattle, Washington 98195-7280, USA.</mods:affiliation><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Pharmacology, University of Washington, Seattle, Washington 98195-7280</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:E1849B510BC94574DFAE4468322D17AEDD2EC28B</idno><date when="2005" year="2005">2005</date><idno type="doi">10.1038/nrn1587</idno><idno type="url">https://api.istex.fr/document/E1849B510BC94574DFAE4468322D17AEDD2EC28B/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001716</idno><idno type="wicri:Area/Main/Curation">001480</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Modulation of neurodegeneration by molecular chaperones</title><author><name sortKey="Muchowski, Paul J" sort="Muchowski, Paul J" uniqKey="Muchowski P" first="Paul J." last="Muchowski">Paul J. 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Wacker</name><affiliation wicri:level="1"><mods:affiliation>Department of Pharmacology, University of Washington, Seattle, Washington 98195-7280, USA.</mods:affiliation><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Pharmacology, University of Washington, Seattle, Washington 98195-7280</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j">Nature Reviews Neuroscience</title><idno type="ISSN">1471-003X</idno><idno type="eISSN">1471-0048</idno><imprint><publisher>Nature Publishing Group</publisher><date type="published" when="2005-01">2005-01</date><biblScope unit="volume">6</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="11">11</biblScope><biblScope unit="page" to="22">22</biblScope></imprint><idno type="ISSN">1471-003X</idno></series><idno type="istex">E1849B510BC94574DFAE4468322D17AEDD2EC28B</idno><idno type="DOI">10.1038/nrn1587</idno><idno type="ArticleID">nrn1587</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1471-003X</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="eng">Many neurodegenerative disorders are characterized by conformational changes in proteins that result in misfolding, aggregation and intra- or extra-neuronal accumulation of amyloid fibrils. Molecular chaperones provide a first line of defence against misfolded, aggregation-prone proteins and are among the most potent suppressors of neurodegeneration known for animal models of human disease. Recent studies have investigated the role of molecular chaperones in amyotrophic lateral sclerosis, Alzheimer's disease, Parkinson's disease and polyglutamine diseases. We propose that molecular chaperones are neuroprotective because of their ability to modulate the earliest aberrant protein interactions that trigger pathogenic cascades. A detailed understanding of the molecular basis of chaperone-mediated protection against neurodegeneration might lead to the development of therapies for neurodegenerative disorders that are associated with protein misfolding and aggregation.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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