Neurogenetics II: complex disorders
Identifieur interne : 001357 ( Main/Corpus ); précédent : 001356; suivant : 001358Neurogenetics II: complex disorders
Auteurs : A F WrightSource :
- Journal of Neurology, Neurosurgery & Psychiatry [ 0022-3050 ] ; 2005-05.
English descriptors
- KwdEn :
- ALS, amyotrophic lateral sclerosis, APP, amyloid β protein precursor, ASPs, affected sib pairs, Alzheimer’s disease, CD/CV, common disease/common variant, CD/RV, common disease/rare variant, CSF, cerebral spinal fluid, FAD, familial Alzheimer disease, FPD, familial Parkinson disease, FTD, fronto-temporal lobe dementia, IBD, identical by descent, LD, linkage disequilibrium, MS, multiple sclerosis, NFD, neurofibrillary degeneration, PHF, paired helical filament, Parkinson’s disease, QT, quantitative trait, SN, substantia nigra, SNP, single nucleotide polymorphism, SOD1, superoxide dismutase 1, genetics.
Abstract
The genetic analysis of common neurological disorders will be a difficult and protracted endeavour. Genetics is only one of many disciplines that will be required but it has already thrown considerable light on the aetiology of several major neurological disorders through the analysis of rare inherited subgroups. The identification of individual susceptibility genes with variants of smaller effect will be more difficult but there is no sharp demarcation between large and small genetic effects, so that many new and important insights will emerge using existing and new technologies. The availability of improved neuroimaging, better animal models of disease and new genetic tools, such as high-throughput gene chips, expression microarrays and proteomics, are extending the range of traditional genetic mapping tools. Finally, an understanding of the genetic and epigenetic mechanisms that restrain the differentiation and integration of human neural stem cells into mature neuronal networks could have a major impact on clinical practice. These approaches will be illustrated in the context of Alzheimer disease, Parkinson disease and synucleinopathies, tauopathies, amyotrophic lateral sclerosis and stroke.
Url:
DOI: 10.1136/jnnp.2004.047704
Links to Exploration step
ISTEX:C0826A8812E849059C71430D6F57B97902569950Le document en format XML
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Genetics is only one of many disciplines that will be required but it has already thrown considerable light on the aetiology of several major neurological disorders through the analysis of rare inherited subgroups. The identification of individual susceptibility genes with variants of smaller effect will be more difficult but there is no sharp demarcation between large and small genetic effects, so that many new and important insights will emerge using existing and new technologies. The availability of improved neuroimaging, better animal models of disease and new genetic tools, such as high-throughput gene chips, expression microarrays and proteomics, are extending the range of traditional genetic mapping tools. Finally, an understanding of the genetic and epigenetic mechanisms that restrain the differentiation and integration of human neural stem cells into mature neuronal networks could have a major impact on clinical practice. These approaches will be illustrated in the context of Alzheimer disease, Parkinson disease and synucleinopathies, tauopathies, amyotrophic lateral sclerosis and stroke.</div></front></TEI><istex><corpusName>bmj</corpusName><author><json:item><name>A F Wright</name></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Review</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Memory disorders (neurology)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Drugs: CNS (not psychiatric)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Motor neurone disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Neuromuscular disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Spinal cord</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Stroke</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Memory disorders (psychiatry)</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Psychiatry of old age</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ALS, amyotrophic lateral sclerosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>APP, amyloid β protein precursor</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ASPs, affected sib pairs</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CD/CV, common disease/common variant</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CD/RV, common disease/rare variant</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>CSF, cerebral spinal fluid</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>FAD, familial Alzheimer disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>FPD, familial Parkinson disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>FTD, fronto-temporal lobe dementia</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>IBD, identical by descent</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>LD, linkage disequilibrium</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>MS, multiple sclerosis</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>NFD, neurofibrillary degeneration</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PHF, paired helical filament</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>QT, quantitative trait</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SN, substantia nigra</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SNP, single nucleotide polymorphism</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>SOD1, superoxide dismutase 1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Alzheimer’s disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson’s disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>genetics</value></json:item></subject><language><json:string>eng</json:string></language><abstract>The genetic analysis of common neurological disorders will be a difficult and protracted endeavour. Genetics is only one of many disciplines that will be required but it has already thrown considerable light on the aetiology of several major neurological disorders through the analysis of rare inherited subgroups. The identification of individual susceptibility genes with variants of smaller effect will be more difficult but there is no sharp demarcation between large and small genetic effects, so that many new and important insights will emerge using existing and new technologies. The availability of improved neuroimaging, better animal models of disease and new genetic tools, such as high-throughput gene chips, expression microarrays and proteomics, are extending the range of traditional genetic mapping tools. Finally, an understanding of the genetic and epigenetic mechanisms that restrain the differentiation and integration of human neural stem cells into mature neuronal networks could have a major impact on clinical practice. These approaches will be illustrated in the context of Alzheimer disease, Parkinson disease and synucleinopathies, tauopathies, amyotrophic lateral sclerosis and stroke.</abstract><qualityIndicators><score>7.076</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>false</refBibsNative><keywordCount>31</keywordCount><abstractCharCount>1214</abstractCharCount><pdfWordCount>7896</pdfWordCount><pdfCharCount>51029</pdfCharCount><pdfPageCount>9</pdfPageCount><abstractWordCount>173</abstractWordCount></qualityIndicators><title>Neurogenetics II: complex disorders</title><pmid><json:string>15834017</json:string></pmid><genre><json:string>review-article</json:string></genre><host><volume>76</volume><pages><first>623</first></pages><issn><json:string>0022-3050</json:string></issn><issue>5</issue><genre></genre><language><json:string>unknown</json:string></language><eissn><json:string>1468-330X</json:string></eissn><title>Journal of Neurology, Neurosurgery & Psychiatry</title></host><publicationDate>2005</publicationDate><copyrightDate>2005</copyrightDate><doi><json:string>10.1136/jnnp.2004.047704</json:string></doi><id>C0826A8812E849059C71430D6F57B97902569950</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/C0826A8812E849059C71430D6F57B97902569950/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/C0826A8812E849059C71430D6F57B97902569950/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/C0826A8812E849059C71430D6F57B97902569950/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Neurogenetics II: complex disorders</title><respStmt xml:id="ISTEX-API" resp="Références bibliographiques récupérées via GROBID" name="ISTEX-API (INIST-CNRS)"></respStmt></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>BMJ Publishing Group Ltd</publisher><availability><p>BMJ</p></availability><date>2005-04-15</date></publicationStmt><notesStmt><note>Correspondence to:
A F Wright
MRC Human Genetics Unit, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK; alan.wright@hgu.mrc.ac.uk</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Neurogenetics II: complex disorders</title><author><persName><forename type="first">A F</forename><surname>Wright</surname></persName></author></analytic><monogr><title level="j">Journal of Neurology, Neurosurgery & Psychiatry</title><title level="j" type="abbrev">J Neurol Neurosurg Psychiatry</title><idno type="pISSN">0022-3050</idno><idno type="eISSN">1468-330X</idno><imprint><publisher>BMJ Publishing Group Ltd</publisher><date type="published" when="2005-05"></date><biblScope unit="volume">76</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="623">623</biblScope></imprint></monogr><idno type="istex">C0826A8812E849059C71430D6F57B97902569950</idno><idno type="DOI">10.1136/jnnp.2004.047704</idno><idno type="href">jnnp-76-623.pdf</idno><idno type="PMID">15834017</idno><idno type="local">0760623</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2005-04-15</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>The genetic analysis of common neurological disorders will be a difficult and protracted endeavour. Genetics is only one of many disciplines that will be required but it has already thrown considerable light on the aetiology of several major neurological disorders through the analysis of rare inherited subgroups. The identification of individual susceptibility genes with variants of smaller effect will be more difficult but there is no sharp demarcation between large and small genetic effects, so that many new and important insights will emerge using existing and new technologies. The availability of improved neuroimaging, better animal models of disease and new genetic tools, such as high-throughput gene chips, expression microarrays and proteomics, are extending the range of traditional genetic mapping tools. Finally, an understanding of the genetic and epigenetic mechanisms that restrain the differentiation and integration of human neural stem cells into mature neuronal networks could have a major impact on clinical practice. These approaches will be illustrated in the context of Alzheimer disease, Parkinson disease and synucleinopathies, tauopathies, amyotrophic lateral sclerosis and stroke.</p></abstract><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>Memory disorders (neurology)</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>Drugs: CNS (not psychiatric)</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>Motor neurone disease</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>Neuromuscular disease</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>Parkinson's disease</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>Spinal cord</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>Stroke</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>Memory disorders (psychiatry)</term></item></list></keywords></textClass><textClass><keywords scheme="keyword"><list><head>hwp-journal-coll</head><item><term>Psychiatry of old age</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>ABR</head><item><term>ALS, amyotrophic lateral sclerosis</term></item><item><term>APP, amyloid β protein precursor</term></item><item><term>ASPs, affected sib pairs</term></item><item><term>CD/CV, common disease/common variant</term></item><item><term>CD/RV, common disease/rare variant</term></item><item><term>CSF, cerebral spinal fluid</term></item><item><term>FAD, familial Alzheimer disease</term></item><item><term>FPD, familial Parkinson disease</term></item><item><term>FTD, fronto-temporal lobe dementia</term></item><item><term>IBD, identical by descent</term></item><item><term>LD, linkage disequilibrium</term></item><item><term>MS, multiple sclerosis</term></item><item><term>NFD, neurofibrillary degeneration</term></item><item><term>PHF, paired helical filament</term></item><item><term>QT, quantitative trait</term></item><item><term>SN, substantia nigra</term></item><item><term>SNP, single nucleotide polymorphism</term></item><item><term>SOD1, superoxide dismutase 1</term></item></list></keywords></textClass><textClass xml:lang="en"><keywords scheme="keyword"><list><head>KWD</head><item><term>Alzheimer’s disease</term></item><item><term>Parkinson’s disease</term></item><item><term>genetics</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2005-04-15">Created</change><change when="2005-05">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-14">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/C0826A8812E849059C71430D6F57B97902569950/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="corpus bmj" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="no"</istex:xmlDeclaration><istex:docType PUBLIC="-//NLM//DTD Journal Archiving and Interchange DTD v2.3 20070202//EN" URI="archivearticle.dtd" name="istex:docType"></istex:docType><istex:document><article xml:lang="en" article-type="review-article"><front><journal-meta><journal-id journal-id-type="hwp">jnnp</journal-id><journal-id journal-id-type="nlm-ta">J Neurol Neurosurg Psychiatry</journal-id><journal-title>Journal of Neurology, Neurosurgery & Psychiatry</journal-title><abbrev-journal-title abbrev-type="publisher">J Neurol Neurosurg Psychiatry</abbrev-journal-title><issn pub-type="ppub">0022-3050</issn><issn pub-type="epub">1468-330X</issn><publisher><publisher-name>BMJ Publishing Group Ltd</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="other">0760623</article-id><article-id pub-id-type="doi">10.1136/jnnp.2004.047704</article-id><article-id pub-id-type="other">jnnp;76/5/623</article-id><article-id pub-id-type="pmid">15834017</article-id><article-id pub-id-type="other">623</article-id><article-id pub-id-type="other">jnnp.2004.047704</article-id><article-categories><subj-group subj-group-type="heading"><subject content-type="original">Review</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Memory disorders (neurology)</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Drugs: CNS (not psychiatric)</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Motor neurone disease</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Neuromuscular disease</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Parkinson's disease</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Spinal cord</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Stroke</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Memory disorders (psychiatry)</subject></subj-group><subj-group subj-group-type="hwp-journal-coll"><subject>Psychiatry of old age</subject></subj-group></article-categories><title-group><article-title>Neurogenetics II: complex disorders</article-title></title-group><contrib-group><contrib contrib-type="author" xlink:type="simple"><name name-style="western"><surname>Wright</surname><given-names>A F</given-names></name></contrib></contrib-group><author-notes><corresp>Correspondence to:
A F Wright
MRC Human Genetics Unit, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK; <ext-link xlink:href="alan.wrighthgu.mrc.ac.uk" ext-link-type="email" xlink:type="simple">alan.wright@hgu.mrc.ac.uk</ext-link></corresp></author-notes><pub-date pub-type="ppub"><month>5</month><year>2005</year></pub-date><pub-date pub-type="epub"><day>15</day><month>4</month><year>2005</year></pub-date><volume>76</volume><volume-id pub-id-type="other">76</volume-id><volume-id pub-id-type="other">76</volume-id><issue>5</issue><issue-id pub-id-type="other">jnnp;76/5</issue-id><issue-id pub-id-type="other">5</issue-id><issue-id pub-id-type="other">76/5</issue-id><fpage>623</fpage><history><date date-type="accepted"><day>08</day><month>11</month><year>2004</year></date><date date-type="received"><day>15</day><month>06</month><year>2004</year></date><date date-type="rev-recd"><day>19</day><month>10</month><year>2004</year></date></history><permissions><copyright-statement>Copyright 2005 Journal of Neurology Neurosurgery and Psychiatry</copyright-statement><copyright-year>2005</copyright-year></permissions><self-uri content-type="pdf" xlink:role="full-text" xlink:href="jnnp-76-623.pdf"></self-uri><abstract xml:lang="en"><p>The genetic analysis of common neurological disorders will be a difficult and protracted endeavour. Genetics is only one of many disciplines that will be required but it has already thrown considerable light on the aetiology of several major neurological disorders through the analysis of rare inherited subgroups. The identification of individual susceptibility genes with variants of smaller effect will be more difficult but there is no sharp demarcation between large and small genetic effects, so that many new and important insights will emerge using existing and new technologies. The availability of improved neuroimaging, better animal models of disease and new genetic tools, such as high-throughput gene chips, expression microarrays and proteomics, are extending the range of traditional genetic mapping tools. Finally, an understanding of the genetic and epigenetic mechanisms that restrain the differentiation and integration of human neural stem cells into mature neuronal networks could have a major impact on clinical practice. These approaches will be illustrated in the context of Alzheimer disease, Parkinson disease and synucleinopathies, tauopathies, amyotrophic lateral sclerosis and stroke.</p></abstract><kwd-group kwd-group-type="ABR" xml:lang="en"><kwd>ALS, amyotrophic lateral sclerosis</kwd><kwd>APP, amyloid β protein precursor</kwd><kwd>ASPs, affected sib pairs</kwd><kwd>CD/CV, common disease/common variant</kwd><kwd>CD/RV, common disease/rare variant</kwd><kwd>CSF, cerebral spinal fluid</kwd><kwd>FAD, familial Alzheimer disease</kwd><kwd>FPD, familial Parkinson disease</kwd><kwd>FTD, fronto-temporal lobe dementia</kwd><kwd>IBD, identical by descent</kwd><kwd>LD, linkage disequilibrium</kwd><kwd>MS, multiple sclerosis</kwd><kwd>NFD, neurofibrillary degeneration</kwd><kwd>PHF, paired helical filament</kwd><kwd>QT, quantitative trait</kwd><kwd>SN, substantia nigra</kwd><kwd>SNP, single nucleotide polymorphism</kwd><kwd>SOD1, superoxide dismutase 1</kwd></kwd-group><kwd-group kwd-group-type="KWD" xml:lang="en"><kwd>Alzheimer’s disease</kwd><kwd>Parkinson’s disease</kwd><kwd>genetics</kwd></kwd-group></article-meta></front></article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Neurogenetics II: complex disorders</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Neurogenetics II: complex disorders</title></titleInfo><name type="personal"><namePart type="given">A F</namePart><namePart type="family">Wright</namePart></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="review-article"></genre><subject><genre>hwp-journal-coll</genre><topic>Memory disorders (neurology)</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Drugs: CNS (not psychiatric)</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Motor neurone disease</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Neuromuscular disease</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Parkinson's disease</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Spinal cord</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Stroke</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Memory disorders (psychiatry)</topic></subject><subject><genre>hwp-journal-coll</genre><topic>Psychiatry of old age</topic></subject><originInfo><publisher>BMJ Publishing Group Ltd</publisher><dateIssued encoding="w3cdtf">2005-05</dateIssued><dateCreated encoding="w3cdtf">2005-04-15</dateCreated><copyrightDate encoding="w3cdtf">2005</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">The genetic analysis of common neurological disorders will be a difficult and protracted endeavour. Genetics is only one of many disciplines that will be required but it has already thrown considerable light on the aetiology of several major neurological disorders through the analysis of rare inherited subgroups. The identification of individual susceptibility genes with variants of smaller effect will be more difficult but there is no sharp demarcation between large and small genetic effects, so that many new and important insights will emerge using existing and new technologies. The availability of improved neuroimaging, better animal models of disease and new genetic tools, such as high-throughput gene chips, expression microarrays and proteomics, are extending the range of traditional genetic mapping tools. Finally, an understanding of the genetic and epigenetic mechanisms that restrain the differentiation and integration of human neural stem cells into mature neuronal networks could have a major impact on clinical practice. These approaches will be illustrated in the context of Alzheimer disease, Parkinson disease and synucleinopathies, tauopathies, amyotrophic lateral sclerosis and stroke.</abstract><note type="author-notes">Correspondence to:
A F Wright
MRC Human Genetics Unit, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK; alan.wright@hgu.mrc.ac.uk</note><subject lang="en"><genre>ABR</genre><topic>ALS, amyotrophic lateral sclerosis</topic><topic>APP, amyloid β protein precursor</topic><topic>ASPs, affected sib pairs</topic><topic>CD/CV, common disease/common variant</topic><topic>CD/RV, common disease/rare variant</topic><topic>CSF, cerebral spinal fluid</topic><topic>FAD, familial Alzheimer disease</topic><topic>FPD, familial Parkinson disease</topic><topic>FTD, fronto-temporal lobe dementia</topic><topic>IBD, identical by descent</topic><topic>LD, linkage disequilibrium</topic><topic>MS, multiple sclerosis</topic><topic>NFD, neurofibrillary degeneration</topic><topic>PHF, paired helical filament</topic><topic>QT, quantitative trait</topic><topic>SN, substantia nigra</topic><topic>SNP, single nucleotide polymorphism</topic><topic>SOD1, superoxide dismutase 1</topic></subject><subject lang="en"><genre>KWD</genre><topic>Alzheimer’s disease</topic><topic>Parkinson’s disease</topic><topic>genetics</topic></subject><relatedItem type="host"><titleInfo><title>Journal of Neurology, Neurosurgery & Psychiatry</title></titleInfo><titleInfo type="abbreviated"><title>J Neurol Neurosurg Psychiatry</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0022-3050</identifier><identifier type="eISSN">1468-330X</identifier><identifier type="PublisherID-hwp">jnnp</identifier><identifier type="PublisherID-nlm-ta">J Neurol Neurosurg Psychiatry</identifier><part><date>2005</date><detail type="volume"><caption>vol.</caption><number>76</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>623</start></extent></part></relatedItem><identifier type="istex">C0826A8812E849059C71430D6F57B97902569950</identifier><identifier type="DOI">10.1136/jnnp.2004.047704</identifier><identifier type="href">jnnp-76-623.pdf</identifier><identifier type="PMID">15834017</identifier><identifier type="local">0760623</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright 2005 Journal of Neurology Neurosurgery and Psychiatry</accessCondition><recordInfo><recordContentSource>BMJ</recordContentSource></recordInfo></mods></metadata><annexes><json:item><original>true</original><mimetype>image/jpeg</mimetype><extension>jpeg</extension><uri>https://api.istex.fr/document/C0826A8812E849059C71430D6F57B97902569950/annexes/jpeg</uri></json:item></annexes><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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