Advances in genetic models of Parkinson's disease
Identifieur interne : 001B12 ( Main/Exploration ); précédent : 001B11; suivant : 001B13Advances in genetic models of Parkinson's disease
Auteurs : Michael K. Lee [États-Unis] ; Donald L. Price [États-Unis]Source :
- Clinical Neuroscience Research [ 1566-2772 ] ; 2001.
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Abstract
Parkinson's disease (PD) is the second most common neurological cause of death, after Alzheimer's disease, in elderly people. PD is characterized by a variety of motoric dysfunctions resulting from the loss of striatal dopamine, which accompany progressive degeneration of dopaminergic neurons in the substantia nigra. While the causes of PD remain elusive in most cases, recent molecular genetic studies have linked mutations in the α-synuclein gene with a rare form of familial PD and mutations in the parkins gene with an autosomal recessive form of familial PD. Identification of these genes is allowing for creation of genetic models where in vivo degenerative processes can be studied. In particular, various transgenic animals expressing human α-synuclein variants have demonstrated that α-synuclein abnormalities can lead to neurodegenerative changes in vivo. These and other genetic models of nigrostriatal degeneration will allow investigators to define in vivo cellular mechanisms that are relevant to PD pathogenesis.
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DOI: 10.1016/S1566-2772(01)00024-X
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Price</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:66444ACBD44168F34CFABFF8A3139971527F99D2</idno><date when="2001" year="2001">2001</date><idno type="doi">10.1016/S1566-2772(01)00024-X</idno><idno type="url">https://api.istex.fr/document/66444ACBD44168F34CFABFF8A3139971527F99D2/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001201</idno><idno type="wicri:Area/Main/Curation">001002</idno><idno type="wicri:Area/Main/Exploration">001B12</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Advances in genetic models of Parkinson's disease</title><author><name sortKey="Lee, Michael K" sort="Lee, Michael K" uniqKey="Lee M" first="Michael K." last="Lee">Michael K. Lee</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Neuropathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation><affiliation><wicri:noCountry code="subField">777</wicri:noCountry></affiliation><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation></author><author><name sortKey="Price, Donald L" sort="Price, Donald L" uniqKey="Price D" first="Donald L." last="Price">Donald L. Price</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Division of Neuropathology, The Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Clinical Neuroscience Research</title><title level="j" type="abbrev">CLIRES</title><idno type="ISSN">1566-2772</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2001">2001</date><biblScope unit="volume">1</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="456">456</biblScope><biblScope unit="page" to="466">466</biblScope></imprint><idno type="ISSN">1566-2772</idno></series><idno type="istex">66444ACBD44168F34CFABFF8A3139971527F99D2</idno><idno type="DOI">10.1016/S1566-2772(01)00024-X</idno><idno type="PII">S1566-2772(01)00024-X</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1566-2772</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Lewy body</term><term>Neurodegeneration</term><term>Parkinson's disease</term><term>Synuclein</term><term>Synucleinopathy</term><term>Transgenic flies</term><term>Transgenic mice</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson's disease (PD) is the second most common neurological cause of death, after Alzheimer's disease, in elderly people. PD is characterized by a variety of motoric dysfunctions resulting from the loss of striatal dopamine, which accompany progressive degeneration of dopaminergic neurons in the substantia nigra. While the causes of PD remain elusive in most cases, recent molecular genetic studies have linked mutations in the α-synuclein gene with a rare form of familial PD and mutations in the parkins gene with an autosomal recessive form of familial PD. Identification of these genes is allowing for creation of genetic models where in vivo degenerative processes can be studied. In particular, various transgenic animals expressing human α-synuclein variants have demonstrated that α-synuclein abnormalities can lead to neurodegenerative changes in vivo. These and other genetic models of nigrostriatal degeneration will allow investigators to define in vivo cellular mechanisms that are relevant to PD pathogenesis.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Lee, Michael K" sort="Lee, Michael K" uniqKey="Lee M" first="Michael K." last="Lee">Michael K. Lee</name></region><name sortKey="Lee, Michael K" sort="Lee, Michael K" uniqKey="Lee M" first="Michael K." last="Lee">Michael K. Lee</name><name sortKey="Lee, Michael K" sort="Lee, Michael K" uniqKey="Lee M" first="Michael K." last="Lee">Michael K. Lee</name><name sortKey="Price, Donald L" sort="Price, Donald L" uniqKey="Price D" first="Donald L." last="Price">Donald L. Price</name><name sortKey="Price, Donald L" sort="Price, Donald L" uniqKey="Price D" first="Donald L." last="Price">Donald L. Price</name><name sortKey="Price, Donald L" sort="Price, Donald L" uniqKey="Price D" first="Donald L." last="Price">Donald L. Price</name><name sortKey="Price, Donald L" sort="Price, Donald L" uniqKey="Price D" first="Donald L." last="Price">Donald L. Price</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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