Parkinson's disease: the genetics of a heterogeneous disorder
Identifieur interne : 000320 ( Main/Corpus ); précédent : 000319; suivant : 000321Parkinson's disease: the genetics of a heterogeneous disorder
Auteurs : D. Gosal ; O. A. Ross ; M. ToftSource :
- European Journal of Neurology [ 1351-5101 ] ; 2006-06.
English descriptors
- KwdEn :
Abstract
Since the first description of Parkinson's disease (PD) in 1817 attempts have been made to resolve the etiology of this common neurodegenerative disorder. In the last century the influence of heredity in PD was controversial. The identification of mutations in six genes responsible for Mendelian forms of PD; α‐synuclein (SNCA), parkin (PRKN), ubiquitin C‐terminal hydrolase L1 (UCH‐L1), oncogene DJ‐1, PTEN‐induced putative kinase 1 (PINK1), and most recently leucine‐rich repeat kinase 2 (LRRK2), has confirmed the role of genetics in familial forms of the disease. The exact relationship of these familial disorders and related genes to the more common sporadic form is currently uncertain. The identification of LRRK2 mutations and the association of common variants in SNCA and UCH‐L1 in apparently sporadic late‐onset disease indicate these genes may be of greater importance than previously believed. The protein products of the six genes are involved in different pathways of neurodegeneration and have opened new avenues of research. This focused research will lead to the development of novel targeted therapies, which may revolutionize the treatment of PD for a substantial proportion of patients.
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DOI: 10.1111/j.1468-1331.2006.01336.x
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Gosal, O. A. Ross and M. Toft</title><title type="short">Parkinson's disease: the genetics of a heterogeneous disorder</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1"><personName><givenNames>D.</givenNames><familyName>Gosal</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a2"><personName><givenNames>O. A.</givenNames><familyName>Ross</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a2 #a3"><personName><givenNames>M.</givenNames><familyName>Toft</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1" countryCode="IE"><unparsedAffiliation>Department of Neurology, Mater Misericordiae University Hospital, Dublin, Ireland</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="US"><unparsedAffiliation>Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL, USA</unparsedAffiliation></affiliation><affiliation xml:id="a3" countryCode="NO"><unparsedAffiliation>Department of Neuroscience, Norwegian University of Science and Technology, Trondheim, Norway</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">genetics</keyword><keyword xml:id="k2">neurodegeneration</keyword><keyword xml:id="k3">Parkinson's disease</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Since the first description of Parkinson's disease (PD) in 1817 attempts have been made to resolve the etiology of this common neurodegenerative disorder. In the last century the influence of heredity in PD was controversial. The identification of mutations in six genes responsible for Mendelian forms of PD; <i>α</i>‐<i>synuclein</i> (<i>SNCA</i>), <i>parkin</i> (<i>PRKN</i>), <i>ubiquitin C‐terminal hydrolase L1</i> (<i>UCH‐L1</i>), oncogene <i>DJ‐1</i>, <i>PTEN‐induced putative kinase 1</i> (<i>PINK1</i>), and most recently <i>leucine‐rich repeat kinase 2</i> (<i>LRRK2</i>), has confirmed the role of genetics in familial forms of the disease. The exact relationship of these familial disorders and related genes to the more common sporadic form is currently uncertain. The identification of <i>LRRK2</i> mutations and the association of common variants in <i>SNCA</i> and <i>UCH‐L1</i> in apparently sporadic late‐onset disease indicate these genes may be of greater importance than previously believed. The protein products of the six genes are involved in different pathways of neurodegeneration and have opened new avenues of research. This focused research will lead to the development of novel targeted therapies, which may revolutionize the treatment of PD for a substantial proportion of patients.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Parkinson's disease: the genetics of a heterogeneous disorder</title></titleInfo><titleInfo type="abbreviated"><title>Parkinson's disease: the genetics of a heterogeneous disorder</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Parkinson's disease: the genetics of a heterogeneous disorder</title></titleInfo><name type="personal"><namePart type="given">D.</namePart><namePart type="family">Gosal</namePart><affiliation>Department of Neurology, Mater Misericordiae University Hospital, Dublin, Ireland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">O. A.</namePart><namePart type="family">Ross</namePart><affiliation>Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="family">Toft</namePart><affiliation>Department of Neuroscience, Mayo Clinic College of Medicine, Jacksonville, FL, USA</affiliation><affiliation>Department of Neuroscience, Norwegian University of Science and Technology, Trondheim, Norway</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><place><placeTerm type="text">Oxford, UK</placeTerm></place><dateIssued encoding="w3cdtf">2006-06</dateIssued><edition>Received 9 May 2005 Accepted 11 July 2005</edition><copyrightDate encoding="w3cdtf">2006</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">4</extent><extent unit="tables">1</extent></physicalDescription><abstract lang="en">Since the first description of Parkinson's disease (PD) in 1817 attempts have been made to resolve the etiology of this common neurodegenerative disorder. In the last century the influence of heredity in PD was controversial. The identification of mutations in six genes responsible for Mendelian forms of PD; α‐synuclein (SNCA), parkin (PRKN), ubiquitin C‐terminal hydrolase L1 (UCH‐L1), oncogene DJ‐1, PTEN‐induced putative kinase 1 (PINK1), and most recently leucine‐rich repeat kinase 2 (LRRK2), has confirmed the role of genetics in familial forms of the disease. The exact relationship of these familial disorders and related genes to the more common sporadic form is currently uncertain. The identification of LRRK2 mutations and the association of common variants in SNCA and UCH‐L1 in apparently sporadic late‐onset disease indicate these genes may be of greater importance than previously believed. The protein products of the six genes are involved in different pathways of neurodegeneration and have opened new avenues of research. This focused research will lead to the development of novel targeted therapies, which may revolutionize the treatment of PD for a substantial proportion of patients.</abstract><subject lang="en"><genre>Keywords</genre><topic>genetics</topic><topic>neurodegeneration</topic><topic>Parkinson's disease</topic></subject><relatedItem type="host"><titleInfo><title>European Journal of Neurology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">1351-5101</identifier><identifier type="eISSN">1468-1331</identifier><identifier type="DOI">10.1111/(ISSN)1468-1331</identifier><identifier type="PublisherID">ENE</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><detail type="issue"><caption>no.</caption><number>6</number></detail><extent unit="pages"><start>616</start><end>627</end><total>12</total></extent></part></relatedItem><identifier type="istex">A6AF88A47101E26E88320C035288C78EF7D5ED7A</identifier><identifier type="DOI">10.1111/j.1468-1331.2006.01336.x</identifier><identifier type="ArticleID">ENE1336</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Ltd</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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