Parkinson's disease
Identifieur interne : 000956 ( Main/Corpus ); précédent : 000955; suivant : 000957Parkinson's disease
Auteurs : Bobby Thomas ; M. Flint BealSource :
- Human Molecular Genetics [ 0964-6906 ] ; 2007-10-15.
Abstract
Parkinson's disease (PD) is a chronic progressive neurodegenerative movement disorder characterized by a profound and selective loss of nigrostriatal dopaminergic neurons. Clinical manifestations of this complex disease include motor impairments involving resting tremor, bradykinesia, postural instability, gait difficulty and rigidity. Current medications only provide symptomatic relief and fail to halt the death of dopaminergic neurons. A major hurdle in development of neuroprotective therapies are due to limited understanding of disease processes leading to death of dopaminergic neurons. While the etiology of dopaminergic neuronal demise is elusive, a combination of genetic susceptibilities and environmental factors seems to play a critical role. The majority of PD cases are sporadic however, the discovery of genes linked to rare familial forms of disease (encoding -synuclein, parkin, DJ-1, PINK-1 and LRRK2) and studies from experimental animal models has provided crucial insights into molecular mechanisms in disease pathogenesis and identified probable targets for therapeutic intervention. Recent findings implicate mitochondrial dysfunction, oxidative damage, abnormal protein accumulation and protein phosphorylation as key molecular mechanisms compromising dopamine neuronal function and survival as the underlying cause of pathogenesis in both sporadic and familial PD. In this review we provide an overview of the most relevant findings made by the PD research community in the last year and discuss how these significant findings improved our understanding of events leading to nigrostriatal dopaminergic degeneration, and identification of potential cell survival pathways that could serve as targets for neuroprotective therapies in preventing this disabling neurological illness.
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DOI: 10.1093/hmg/ddm159
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Flint Beal</name><affiliation><mods:affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, A-501, New York, NY 10021, USA</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:9C9D389ADD64C273974F5B372B1247B71BFC89B3</idno><date when="2007" year="2007">2007</date><idno type="doi">10.1093/hmg/ddm159</idno><idno type="url">https://api.istex.fr/document/9C9D389ADD64C273974F5B372B1247B71BFC89B3/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">000956</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Parkinson's disease</title><author><name sortKey="Thomas, Bobby" sort="Thomas, Bobby" uniqKey="Thomas B" first="Bobby" last="Thomas">Bobby Thomas</name><affiliation><mods:affiliation>E-mail: bot2003@med.cornell.edu</mods:affiliation></affiliation></author><author><name sortKey="Beal, M Flint" sort="Beal, M Flint" uniqKey="Beal M" first="M. 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Flint Beal</name><affiliation><mods:affiliation>Department of Neurology and Neuroscience, Weill Medical College of Cornell University, 525 East 68th Street, A-501, New York, NY 10021, USA</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Human Molecular Genetics</title><idno type="ISSN">0964-6906</idno><idno type="eISSN">1460-2083</idno><imprint><publisher>Oxford University Press</publisher><date type="published" when="2007-10-15">2007-10-15</date><biblScope unit="volume">16</biblScope><biblScope unit="issue">R2</biblScope><biblScope unit="page" from="R183">R183</biblScope><biblScope unit="page" to="R194">R194</biblScope></imprint><idno type="ISSN">0964-6906</idno></series><idno type="istex">9C9D389ADD64C273974F5B372B1247B71BFC89B3</idno><idno type="DOI">10.1093/hmg/ddm159</idno><idno type="ArticleID">ddm159</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0964-6906</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract">Parkinson's disease (PD) is a chronic progressive neurodegenerative movement disorder characterized by a profound and selective loss of nigrostriatal dopaminergic neurons. Clinical manifestations of this complex disease include motor impairments involving resting tremor, bradykinesia, postural instability, gait difficulty and rigidity. Current medications only provide symptomatic relief and fail to halt the death of dopaminergic neurons. A major hurdle in development of neuroprotective therapies are due to limited understanding of disease processes leading to death of dopaminergic neurons. While the etiology of dopaminergic neuronal demise is elusive, a combination of genetic susceptibilities and environmental factors seems to play a critical role. The majority of PD cases are sporadic however, the discovery of genes linked to rare familial forms of disease (encoding -synuclein, parkin, DJ-1, PINK-1 and LRRK2) and studies from experimental animal models has provided crucial insights into molecular mechanisms in disease pathogenesis and identified probable targets for therapeutic intervention. Recent findings implicate mitochondrial dysfunction, oxidative damage, abnormal protein accumulation and protein phosphorylation as key molecular mechanisms compromising dopamine neuronal function and survival as the underlying cause of pathogenesis in both sporadic and familial PD. In this review we provide an overview of the most relevant findings made by the PD research community in the last year and discuss how these significant findings improved our understanding of events leading to nigrostriatal dopaminergic degeneration, and identification of potential cell survival pathways that could serve as targets for neuroprotective therapies in preventing this disabling neurological illness.</div></front></TEI><istex><corpusName>oup</corpusName><author><json:item><name>Bobby Thomas</name><affiliations><json:string>E-mail: bot2003@med.cornell.edu</json:string></affiliations></json:item><json:item><name>M. 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While the etiology of dopaminergic neuronal demise is elusive, a combination of genetic susceptibilities and environmental factors seems to play a critical role. The majority of PD cases are sporadic however, the discovery of genes linked to rare familial forms of disease (encoding -synuclein, parkin, DJ-1, PINK-1 and LRRK2) and studies from experimental animal models has provided crucial insights into molecular mechanisms in disease pathogenesis and identified probable targets for therapeutic intervention. Recent findings implicate mitochondrial dysfunction, oxidative damage, abnormal protein accumulation and protein phosphorylation as key molecular mechanisms compromising dopamine neuronal function and survival as the underlying cause of pathogenesis in both sporadic and familial PD. In this review we provide an overview of the most relevant findings made by the PD research community in the last year and discuss how these significant findings improved our understanding of events leading to nigrostriatal dopaminergic degeneration, and identification of potential cell survival pathways that could serve as targets for neuroprotective therapies in preventing this disabling neurological illness.</abstract><qualityIndicators><score>7.916</score><pdfVersion>1.2</pdfVersion><pdfPageSize>609.675 x 795.005 pts</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>1</keywordCount><abstractCharCount>1808</abstractCharCount><pdfWordCount>10060</pdfWordCount><pdfCharCount>69220</pdfCharCount><pdfPageCount>12</pdfPageCount><abstractWordCount>243</abstractWordCount></qualityIndicators><title>Parkinson's disease</title><genre><json:string>review-article</json:string></genre><host><volume>16</volume><pages><last>R194</last><first>R183</first></pages><issn><json:string>0964-6906</json:string></issn><issue>R2</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1460-2083</json:string></eissn><title>Human Molecular Genetics</title></host><categories><wos><json:string>BIOCHEMISTRY & MOLECULAR BIOLOGY</json:string><json:string>GENETICS & HEREDITY</json:string></wos></categories><publicationDate>2007</publicationDate><copyrightDate>2007</copyrightDate><doi><json:string>10.1093/hmg/ddm159</json:string></doi><id>9C9D389ADD64C273974F5B372B1247B71BFC89B3</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/9C9D389ADD64C273974F5B372B1247B71BFC89B3/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/9C9D389ADD64C273974F5B372B1247B71BFC89B3/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/9C9D389ADD64C273974F5B372B1247B71BFC89B3/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a">Parkinson's disease</title><respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Oxford University Press</publisher><availability><p>OUP</p></availability><date>2007</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Parkinson's disease</title><author><persName><forename type="first">Bobby</forename><surname>Thomas</surname></persName><email>bot2003@med.cornell.edu</email></author><author><persName><forename type="first">M. 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Recent findings implicate mitochondrial dysfunction, oxidative damage, abnormal protein accumulation and protein phosphorylation as key molecular mechanisms compromising dopamine neuronal function and survival as the underlying cause of pathogenesis in both sporadic and familial PD. In this review we provide an overview of the most relevant findings made by the PD research community in the last year and discuss how these significant findings improved our understanding of events leading to nigrostriatal dopaminergic degeneration, and identification of potential cell survival pathways that could serve as targets for neuroprotective therapies in preventing this disabling neurological illness.</p></abstract></profileDesc><revisionDesc><change when="2007-10-15">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-15">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/9C9D389ADD64C273974F5B372B1247B71BFC89B3/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus oup" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Publishing DTD v2.3 20070202//EN" URI="journalpublishing.dtd" name="istex:docType"></istex:docType><istex:document><article article-type="review-article"><front><journal-meta><journal-id journal-id-type="publisher-id">hmg</journal-id><journal-id journal-id-type="hwp">hmg</journal-id><journal-title>Human Molecular Genetics</journal-title><issn pub-type="ppub">0964-6906</issn><issn pub-type="epub">1460-2083</issn><publisher><publisher-name>Oxford University Press</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.1093/hmg/ddm159</article-id><article-id pub-id-type="publisher-id">ddm159</article-id><article-categories><subj-group subj-group-type="heading"><subject>REVIEWS</subject></subj-group></article-categories><title-group><article-title>Parkinson's disease</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Thomas</surname><given-names>Bobby</given-names></name><xref ref-type="corresp" rid="cor1">*</xref></contrib><contrib contrib-type="author"><name><surname>Beal</surname><given-names>M. Flint</given-names></name></contrib></contrib-group><aff><addr-line>Department of Neurology and Neuroscience</addr-line>, <institution>Weill Medical College of Cornell University</institution>, <addr-line>525 East 68th Street, A-501, New York, NY 10021</addr-line>, <country>USA</country></aff><author-notes><corresp id="cor1"><label>*</label>To whom correspondence should be addressed. Tel: <phone>+1 2127465341</phone>; Fax: <fax>+1 2127468276</fax>; Email: <email>bot2003@med.cornell.edu</email></corresp></author-notes><pub-date pub-type="ppub"><day>15</day><month>10</month><year>2007</year></pub-date><volume>16</volume><issue>R2</issue><fpage>R183</fpage><lpage>R194</lpage><history><date date-type="received"><day>30</day><month>5</month><year>2007</year></date><date date-type="rev-recd"><day>30</day><month>5</month><year>2007</year></date><date date-type="accepted"><day>20</day><month>6</month><year>2007</year></date></history><copyright-statement>© The Author 2007. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org</copyright-statement><copyright-year>2007</copyright-year><abstract><p>Parkinson's disease (PD) is a chronic progressive neurodegenerative movement disorder characterized by a profound and selective loss of nigrostriatal dopaminergic neurons. Clinical manifestations of this complex disease include motor impairments involving resting tremor, bradykinesia, postural instability, gait difficulty and rigidity. Current medications only provide symptomatic relief and fail to halt the death of dopaminergic neurons. A major hurdle in development of neuroprotective therapies are due to limited understanding of disease processes leading to death of dopaminergic neurons. While the etiology of dopaminergic neuronal demise is elusive, a combination of genetic susceptibilities and environmental factors seems to play a critical role. The majority of PD cases are sporadic however, the discovery of genes linked to rare familial forms of disease (encoding <italic>α-synuclein</italic>, <italic>parkin</italic>, <italic>DJ-1</italic>, <italic>PINK-1</italic> and <italic>LRRK2</italic>) and studies from experimental animal models has provided crucial insights into molecular mechanisms in disease pathogenesis and identified probable targets for therapeutic intervention. Recent findings implicate mitochondrial dysfunction, oxidative damage, abnormal protein accumulation and protein phosphorylation as key molecular mechanisms compromising dopamine neuronal function and survival as the underlying cause of pathogenesis in both sporadic and familial PD. In this review we provide an overview of the most relevant findings made by the PD research community in the last year and discuss how these significant findings improved our understanding of events leading to nigrostriatal dopaminergic degeneration, and identification of potential cell survival pathways that could serve as targets for neuroprotective therapies in preventing this disabling neurological illness.</p></abstract></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Parkinson's disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">Bobby</namePart><namePart type="family">Thomas</namePart><affiliation>E-mail: bot2003@med.cornell.edu</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M. 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Recent findings implicate mitochondrial dysfunction, oxidative damage, abnormal protein accumulation and protein phosphorylation as key molecular mechanisms compromising dopamine neuronal function and survival as the underlying cause of pathogenesis in both sporadic and familial PD. In this review we provide an overview of the most relevant findings made by the PD research community in the last year and discuss how these significant findings improved our understanding of events leading to nigrostriatal dopaminergic degeneration, and identification of potential cell survival pathways that could serve as targets for neuroprotective therapies in preventing this disabling neurological illness.</abstract><relatedItem type="host"><titleInfo><title>Human Molecular Genetics</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0964-6906</identifier><identifier type="eISSN">1460-2083</identifier><identifier type="PublisherID">hmg</identifier><identifier type="PublisherID-hwp">hmg</identifier><part><date>2007</date><detail type="volume"><caption>vol.</caption><number>16</number></detail><detail type="issue"><caption>no.</caption><number>R2</number></detail><extent unit="pages"><start>R183</start><end>R194</end></extent></part></relatedItem><identifier type="istex">9C9D389ADD64C273974F5B372B1247B71BFC89B3</identifier><identifier type="DOI">10.1093/hmg/ddm159</identifier><identifier type="ArticleID">ddm159</identifier><accessCondition type="use and reproduction" contentType="copyright">The Author 2007. 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