A molecular basis for the increased vulnerability of substantia nigra dopamine neurons in aging and Parkinson's disease
Identifieur interne : 000840 ( Main/Exploration ); précédent : 000839; suivant : 000841A molecular basis for the increased vulnerability of substantia nigra dopamine neurons in aging and Parkinson's disease
Auteurs : C. Savio Chan [États-Unis] ; Tracy S. Gertler [États-Unis] ; D. James Surmeier [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2010.
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Abstract
Parkinson's disease (PD) is a common neurodegenerative disorder of unknown etiology. There is no cure or proven strategy for slowing the progression of the disease. Although there are signs of pathology in many brain regions, the core symptoms of PD are attributable to the selective degeneration of dopaminergic neurons in the substantia nigra pars compacta. A potential clue to the vulnerability of these neurons is an increasing reliance with age upon L‐type Ca2+ channels with a pore‐forming Cav1.3 subunit to support autonomous activity. This reliance could pose a sustained stress on mitochondrial ATP generating oxidative phosphorylation, accelerating cellular aging and death. Systemic administration of isradipine, a dihydropyridine blocker of these channels, forces dopaminergic neurons in rodents to revert to a juvenile, L‐type Ca2+ channel independent mechanism to generate autonomous activity. This “rejuvenation” confers protection against toxins that produce experimental Parkinsonism, pointing to a potential neuroprotective strategy for PD. Their decades‐long track record of safe use in the treatment of hypertension makes dihydropyridines particularly attractive as a therapeutic tool in PD. © 2010 Movement Disorder Society
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DOI: 10.1002/mds.22801
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Savio Chan</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</wicri:regionArea><placeName><region type="state">Illinois</region></placeName></affiliation></author><author><name sortKey="Gertler, Tracy S" sort="Gertler, Tracy S" uniqKey="Gertler T" first="Tracy S." last="Gertler">Tracy S. Gertler</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</wicri:regionArea><placeName><region type="state">Illinois</region></placeName></affiliation></author><author><name sortKey="Surmeier, D James" sort="Surmeier, D James" uniqKey="Surmeier D" first="D. James" last="Surmeier">D. James Surmeier</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois</wicri:regionArea><placeName><region type="state">Illinois</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</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="2010">2010</date><biblScope unit="volume">25</biblScope><biblScope unit="issue">S1</biblScope><biblScope unit="page" from="S63">S63</biblScope><biblScope unit="page" to="S70">S70</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">F06FD358D4702CA09D2BABC47AC253B64B3C65A1</idno><idno type="DOI">10.1002/mds.22801</idno><idno type="ArticleID">MDS22801</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Parkinson's disease</term><term>aging</term><term>dopamine</term><term>neurons</term><term>substantia nigra</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is a common neurodegenerative disorder of unknown etiology. There is no cure or proven strategy for slowing the progression of the disease. Although there are signs of pathology in many brain regions, the core symptoms of PD are attributable to the selective degeneration of dopaminergic neurons in the substantia nigra pars compacta. A potential clue to the vulnerability of these neurons is an increasing reliance with age upon L‐type Ca2+ channels with a pore‐forming Cav1.3 subunit to support autonomous activity. This reliance could pose a sustained stress on mitochondrial ATP generating oxidative phosphorylation, accelerating cellular aging and death. Systemic administration of isradipine, a dihydropyridine blocker of these channels, forces dopaminergic neurons in rodents to revert to a juvenile, L‐type Ca2+ channel independent mechanism to generate autonomous activity. This “rejuvenation” confers protection against toxins that produce experimental Parkinsonism, pointing to a potential neuroprotective strategy for PD. Their decades‐long track record of safe use in the treatment of hypertension makes dihydropyridines particularly attractive as a therapeutic tool in PD. © 2010 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Illinois</li></region></list><tree><country name="États-Unis"><region name="Illinois"><name sortKey="Chan, C Savio" sort="Chan, C Savio" uniqKey="Chan C" first="C. Savio" last="Chan">C. Savio Chan</name></region><name sortKey="Gertler, Tracy S" sort="Gertler, Tracy S" uniqKey="Gertler T" first="Tracy S." last="Gertler">Tracy S. Gertler</name><name sortKey="Surmeier, D James" sort="Surmeier, D James" uniqKey="Surmeier D" first="D. James" last="Surmeier">D. James Surmeier</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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