Parkinson disease.
Identifieur interne : 000049 ( Main/Exploration ); précédent : 000048; suivant : 000050Parkinson disease.
Auteurs : Werner Poewe [Autriche] ; Klaus Seppi [Autriche] ; Caroline M. Tanner [États-Unis] ; Glenda M. Halliday [Australie] ; Patrik Brundin [États-Unis] ; Jens Volkmann [Allemagne] ; Anette-Eleonore Schrag [Royaume-Uni] ; Anthony E. Lang [Canada]Source :
- Nature reviews. Disease primers [ 2056-676X ] ; 2017.
Abstract
Parkinson disease is the second-most common neurodegenerative disorder that affects 2-3% of the population ≥65 years of age. Neuronal loss in the substantia nigra, which causes striatal dopamine deficiency, and intracellular inclusions containing aggregates of α-synuclein are the neuropathological hallmarks of Parkinson disease. Multiple other cell types throughout the central and peripheral autonomic nervous system are also involved, probably from early disease onwards. Although clinical diagnosis relies on the presence of bradykinesia and other cardinal motor features, Parkinson disease is associated with many non-motor symptoms that add to overall disability. The underlying molecular pathogenesis involves multiple pathways and mechanisms: α-synuclein proteostasis, mitochondrial function, oxidative stress, calcium homeostasis, axonal transport and neuroinflammation. Recent research into diagnostic biomarkers has taken advantage of neuroimaging in which several modalities, including PET, single-photon emission CT (SPECT) and novel MRI techniques, have been shown to aid early and differential diagnosis. Treatment of Parkinson disease is anchored on pharmacological substitution of striatal dopamine, in addition to non-dopaminergic approaches to address both motor and non-motor symptoms and deep brain stimulation for those developing intractable L-DOPA-related motor complications. Experimental therapies have tried to restore striatal dopamine by gene-based and cell-based approaches, and most recently, aggregation and cellular transport of α-synuclein have become therapeutic targets. One of the greatest current challenges is to identify markers for prodromal disease stages, which would allow novel disease-modifying therapies to be started earlier.
DOI: 10.1038/nrdp.2017.13
PubMed: 28332488
Affiliations:
- Allemagne, Australie, Autriche, Canada, Royaume-Uni, États-Unis
- Angleterre, Bavière, Californie, District de Basse-Franconie, Grand Londres, Michigan, Ontario, Tyrol (Land)
- Innsbruck, Londres, Toronto, Wurtzbourg
- Université de Toronto, Université de médecine d'Innsbruck
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Le document en format XML
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Halliday</name><affiliation wicri:level="1"><nlm:affiliation>Brain and Mind Centre, Sydney Medical School, University of Sydney, Sydney, New South Wales, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Brain and Mind Centre, Sydney Medical School, University of Sydney, Sydney, New South Wales</wicri:regionArea><wicri:noRegion>New South Wales</wicri:noRegion></affiliation></author><author><name sortKey="Brundin, Patrik" sort="Brundin, Patrik" uniqKey="Brundin P" first="Patrik" last="Brundin">Patrik Brundin</name><affiliation wicri:level="2"><nlm:affiliation>Van Andel Research Institute, Center for Neurodegenerative Science, Grand Rapids, Michigan, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Van Andel Research Institute, Center for Neurodegenerative Science, Grand Rapids, Michigan</wicri:regionArea><placeName><region type="state">Michigan</region></placeName></affiliation></author><author><name sortKey="Volkmann, Jens" sort="Volkmann, Jens" uniqKey="Volkmann J" first="Jens" last="Volkmann">Jens Volkmann</name><affiliation wicri:level="3"><nlm:affiliation>Department of Neurology, University Hospital of Würzburg, Würzburg, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Neurology, University Hospital of Würzburg, Würzburg</wicri:regionArea><placeName><region type="land" nuts="1">Bavière</region><region type="district" nuts="2">District de Basse-Franconie</region><settlement type="city">Wurtzbourg</settlement></placeName></affiliation></author><author><name sortKey="Schrag, Anette Eleonore" sort="Schrag, Anette Eleonore" uniqKey="Schrag A" first="Anette-Eleonore" last="Schrag">Anette-Eleonore Schrag</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical Neuroscience, UCL Institute of Neurology, London, UK.</nlm:affiliation><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Department of Clinical Neuroscience, 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="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E" last="Lang">Anthony E. Lang</name><affiliation wicri:level="4"><nlm:affiliation>Division of Neurology, Department of Medicine, University of Toronto, Toronto, Ontario, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Department of Medicine, University of Toronto, Toronto, Ontario</wicri:regionArea><orgName type="university">Université de Toronto</orgName><placeName><settlement type="city">Toronto</settlement><region type="state">Ontario</region></placeName></affiliation></author></analytic><series><title level="j">Nature reviews. Disease primers</title><idno type="eISSN">2056-676X</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson disease is the second-most common neurodegenerative disorder that affects 2-3% of the population ≥65 years of age. Neuronal loss in the substantia nigra, which causes striatal dopamine deficiency, and intracellular inclusions containing aggregates of α-synuclein are the neuropathological hallmarks of Parkinson disease. Multiple other cell types throughout the central and peripheral autonomic nervous system are also involved, probably from early disease onwards. Although clinical diagnosis relies on the presence of bradykinesia and other cardinal motor features, Parkinson disease is associated with many non-motor symptoms that add to overall disability. The underlying molecular pathogenesis involves multiple pathways and mechanisms: α-synuclein proteostasis, mitochondrial function, oxidative stress, calcium homeostasis, axonal transport and neuroinflammation. Recent research into diagnostic biomarkers has taken advantage of neuroimaging in which several modalities, including PET, single-photon emission CT (SPECT) and novel MRI techniques, have been shown to aid early and differential diagnosis. Treatment of Parkinson disease is anchored on pharmacological substitution of striatal dopamine, in addition to non-dopaminergic approaches to address both motor and non-motor symptoms and deep brain stimulation for those developing intractable L-DOPA-related motor complications. Experimental therapies have tried to restore striatal dopamine by gene-based and cell-based approaches, and most recently, aggregation and cellular transport of α-synuclein have become therapeutic targets. One of the greatest current challenges is to identify markers for prodromal disease stages, which would allow novel disease-modifying therapies to be started earlier.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Australie</li><li>Autriche</li><li>Canada</li><li>Royaume-Uni</li><li>États-Unis</li></country><region><li>Angleterre</li><li>Bavière</li><li>Californie</li><li>District de Basse-Franconie</li><li>Grand Londres</li><li>Michigan</li><li>Ontario</li><li>Tyrol (Land)</li></region><settlement><li>Innsbruck</li><li>Londres</li><li>Toronto</li><li>Wurtzbourg</li></settlement><orgName><li>Université de Toronto</li><li>Université de médecine d'Innsbruck</li></orgName></list><tree><country name="Autriche"><region name="Tyrol (Land)"><name sortKey="Poewe, Werner" sort="Poewe, Werner" uniqKey="Poewe W" first="Werner" last="Poewe">Werner Poewe</name></region><name sortKey="Seppi, Klaus" sort="Seppi, Klaus" uniqKey="Seppi K" first="Klaus" last="Seppi">Klaus Seppi</name></country><country name="États-Unis"><region name="Californie"><name sortKey="Tanner, Caroline M" sort="Tanner, Caroline M" uniqKey="Tanner C" first="Caroline M" last="Tanner">Caroline M. Tanner</name></region><name sortKey="Brundin, Patrik" sort="Brundin, Patrik" uniqKey="Brundin P" first="Patrik" last="Brundin">Patrik Brundin</name></country><country name="Australie"><noRegion><name sortKey="Halliday, Glenda M" sort="Halliday, Glenda M" uniqKey="Halliday G" first="Glenda M" last="Halliday">Glenda M. Halliday</name></noRegion></country><country name="Allemagne"><region name="Bavière"><name sortKey="Volkmann, Jens" sort="Volkmann, Jens" uniqKey="Volkmann J" first="Jens" last="Volkmann">Jens Volkmann</name></region></country><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Schrag, Anette Eleonore" sort="Schrag, Anette Eleonore" uniqKey="Schrag A" first="Anette-Eleonore" last="Schrag">Anette-Eleonore Schrag</name></region></country><country name="Canada"><region name="Ontario"><name sortKey="Lang, Anthony E" sort="Lang, Anthony E" uniqKey="Lang A" first="Anthony E" last="Lang">Anthony E. 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