Predictors of progression in patients with Friedreich ataxia.
Identifieur interne : 002129 ( PubMed/Checkpoint ); précédent : 002128; suivant : 002130Predictors of progression in patients with Friedreich ataxia.
Auteurs : Alison La Pean [États-Unis] ; Neal Jeffries ; Chelsea Grow ; Bernard Ravina ; Nicholas A. Di ProsperoSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2008.
English descriptors
- KwdEn :
- Adolescent, Adult, Aged, Cardiomyopathies (etiology), Child, Child, Preschool, Confidence Intervals, Dietary Supplements, Disease Progression, Female, Friedreich Ataxia (complications), Friedreich Ataxia (diagnosis), Friedreich Ataxia (genetics), Friedreich Ataxia (therapy), Humans, Interview, Psychological, Male, Membrane Glycoproteins (genetics), Middle Aged, Multivariate Analysis, Predictive Value of Tests, Risk Factors, Scoliosis (etiology), Vitamins (administration & dosage), Young Adult.
- MESH :
- chemical , administration & dosage : Vitamins.
- chemical , genetics : Membrane Glycoproteins.
- complications : Friedreich Ataxia.
- diagnosis : Friedreich Ataxia.
- etiology : Cardiomyopathies, Scoliosis.
- genetics : Friedreich Ataxia.
- therapy : Friedreich Ataxia.
- Adolescent, Adult, Aged, Child, Child, Preschool, Confidence Intervals, Dietary Supplements, Disease Progression, Female, Humans, Interview, Psychological, Male, Middle Aged, Multivariate Analysis, Predictive Value of Tests, Risk Factors, Young Adult.
Abstract
Friedreich ataxia is an inherited, progressive, neurodegenerative disorder that is clinically heterogeneous. It is caused by a trinucleotide (GAA) repeat expansion resulting in frataxin loss and oxidative stress. We assessed clinical features including the development of cardiomyopathy and scoliosis and disease progression including loss of ambulation and interference with activities of daily living relative to the length of the GAA repeat, age of onset, and age of diagnosis in a retrospective cohort study of 61 genetically confirmed patients. The use of antioxidants such as vitamins, dietary supplements, and idebenone was also examined. Linear regression and Cox proportional hazard models assessed predictors to disease milestones. The shorter GAA allele accounted for part of the variability in the age of diagnosis (46%) and less in the age of onset (27%). Multivariate analysis demonstrated that age at diagnosis, which may incorporate other genetic and environmental factors, is more important than GAA length in predicting cardiomyopathy, scoliosis, and disease progression.
DOI: 10.1002/mds.22248
PubMed: 18759347
Affiliations:
Links toward previous steps (curation, corpus...)
Links to Exploration step
pubmed:18759347Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Predictors of progression in patients with Friedreich ataxia.</title><author><name sortKey="La Pean, Alison" sort="La Pean, Alison" uniqKey="La Pean A" first="Alison" last="La Pean">Alison La Pean</name><affiliation wicri:level="1"><nlm:affiliation>Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland 20892-3705, USA. lapeana@ninds.nih.gov</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland 20892-3705</wicri:regionArea><wicri:noRegion>Maryland 20892-3705</wicri:noRegion></affiliation></author><author><name sortKey="Jeffries, Neal" sort="Jeffries, Neal" uniqKey="Jeffries N" first="Neal" last="Jeffries">Neal Jeffries</name></author><author><name sortKey="Grow, Chelsea" sort="Grow, Chelsea" uniqKey="Grow C" first="Chelsea" last="Grow">Chelsea Grow</name></author><author><name sortKey="Ravina, Bernard" sort="Ravina, Bernard" uniqKey="Ravina B" first="Bernard" last="Ravina">Bernard Ravina</name></author><author><name sortKey="Di Prospero, Nicholas A" sort="Di Prospero, Nicholas A" uniqKey="Di Prospero N" first="Nicholas A" last="Di Prospero">Nicholas A. Di Prospero</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2008">2008</date><idno type="doi">10.1002/mds.22248</idno><idno type="RBID">pubmed:18759347</idno><idno type="pmid">18759347</idno><idno type="wicri:Area/PubMed/Corpus">002078</idno><idno type="wicri:Area/PubMed/Curation">002078</idno><idno type="wicri:Area/PubMed/Checkpoint">002129</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Predictors of progression in patients with Friedreich ataxia.</title><author><name sortKey="La Pean, Alison" sort="La Pean, Alison" uniqKey="La Pean A" first="Alison" last="La Pean">Alison La Pean</name><affiliation wicri:level="1"><nlm:affiliation>Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland 20892-3705, USA. lapeana@ninds.nih.gov</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland 20892-3705</wicri:regionArea><wicri:noRegion>Maryland 20892-3705</wicri:noRegion></affiliation></author><author><name sortKey="Jeffries, Neal" sort="Jeffries, Neal" uniqKey="Jeffries N" first="Neal" last="Jeffries">Neal Jeffries</name></author><author><name sortKey="Grow, Chelsea" sort="Grow, Chelsea" uniqKey="Grow C" first="Chelsea" last="Grow">Chelsea Grow</name></author><author><name sortKey="Ravina, Bernard" sort="Ravina, Bernard" uniqKey="Ravina B" first="Bernard" last="Ravina">Bernard Ravina</name></author><author><name sortKey="Di Prospero, Nicholas A" sort="Di Prospero, Nicholas A" uniqKey="Di Prospero N" first="Nicholas A" last="Di Prospero">Nicholas A. Di Prospero</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="eISSN">1531-8257</idno><imprint><date when="2008" type="published">2008</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Cardiomyopathies (etiology)</term><term>Child</term><term>Child, Preschool</term><term>Confidence Intervals</term><term>Dietary Supplements</term><term>Disease Progression</term><term>Female</term><term>Friedreich Ataxia (complications)</term><term>Friedreich Ataxia (diagnosis)</term><term>Friedreich Ataxia (genetics)</term><term>Friedreich Ataxia (therapy)</term><term>Humans</term><term>Interview, Psychological</term><term>Male</term><term>Membrane Glycoproteins (genetics)</term><term>Middle Aged</term><term>Multivariate Analysis</term><term>Predictive Value of Tests</term><term>Risk Factors</term><term>Scoliosis (etiology)</term><term>Vitamins (administration & dosage)</term><term>Young Adult</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Vitamins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Membrane Glycoproteins</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Friedreich Ataxia</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Friedreich Ataxia</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Cardiomyopathies</term><term>Scoliosis</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Friedreich Ataxia</term></keywords><keywords scheme="MESH" qualifier="therapy" xml:lang="en"><term>Friedreich Ataxia</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adolescent</term><term>Adult</term><term>Aged</term><term>Child</term><term>Child, Preschool</term><term>Confidence Intervals</term><term>Dietary Supplements</term><term>Disease Progression</term><term>Female</term><term>Humans</term><term>Interview, Psychological</term><term>Male</term><term>Middle Aged</term><term>Multivariate Analysis</term><term>Predictive Value of Tests</term><term>Risk Factors</term><term>Young Adult</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Friedreich ataxia is an inherited, progressive, neurodegenerative disorder that is clinically heterogeneous. It is caused by a trinucleotide (GAA) repeat expansion resulting in frataxin loss and oxidative stress. We assessed clinical features including the development of cardiomyopathy and scoliosis and disease progression including loss of ambulation and interference with activities of daily living relative to the length of the GAA repeat, age of onset, and age of diagnosis in a retrospective cohort study of 61 genetically confirmed patients. The use of antioxidants such as vitamins, dietary supplements, and idebenone was also examined. Linear regression and Cox proportional hazard models assessed predictors to disease milestones. The shorter GAA allele accounted for part of the variability in the age of diagnosis (46%) and less in the age of onset (27%). Multivariate analysis demonstrated that age at diagnosis, which may incorporate other genetic and environmental factors, is more important than GAA length in predicting cardiomyopathy, scoliosis, and disease progression.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">18759347</PMID><DateCreated><Year>2008</Year><Month>11</Month><Day>04</Day></DateCreated><DateCompleted><Year>2009</Year><Month>04</Month><Day>08</Day></DateCompleted><DateRevised><Year>2015</Year><Month>03</Month><Day>25</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>23</Volume><Issue>14</Issue><PubDate><Year>2008</Year><Month>Oct</Month><Day>30</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Predictors of progression in patients with Friedreich ataxia.</ArticleTitle><Pagination><MedlinePgn>2026-32</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22248</ELocationID><Abstract><AbstractText>Friedreich ataxia is an inherited, progressive, neurodegenerative disorder that is clinically heterogeneous. It is caused by a trinucleotide (GAA) repeat expansion resulting in frataxin loss and oxidative stress. We assessed clinical features including the development of cardiomyopathy and scoliosis and disease progression including loss of ambulation and interference with activities of daily living relative to the length of the GAA repeat, age of onset, and age of diagnosis in a retrospective cohort study of 61 genetically confirmed patients. The use of antioxidants such as vitamins, dietary supplements, and idebenone was also examined. Linear regression and Cox proportional hazard models assessed predictors to disease milestones. The shorter GAA allele accounted for part of the variability in the age of diagnosis (46%) and less in the age of onset (27%). Multivariate analysis demonstrated that age at diagnosis, which may incorporate other genetic and environmental factors, is more important than GAA length in predicting cardiomyopathy, scoliosis, and disease progression.</AbstractText><CopyrightInformation>(c) 2008 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>La Pean</LastName><ForeName>Alison</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Neurogenetics Branch, National Institute of Neurological Disorders and Stroke, NIH, Bethesda, Maryland 20892-3705, USA. lapeana@ninds.nih.gov</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jeffries</LastName><ForeName>Neal</ForeName><Initials>N</Initials></Author><Author ValidYN="Y"><LastName>Grow</LastName><ForeName>Chelsea</ForeName><Initials>C</Initials></Author><Author ValidYN="Y"><LastName>Ravina</LastName><ForeName>Bernard</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Di Prospero</LastName><ForeName>Nicholas A</ForeName><Initials>NA</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>Z01 NS003037-01</GrantID><Agency>Intramural NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052060">Research Support, N.I.H., Intramural</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C093316">GPAA1 protein, human</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008562">Membrane Glycoproteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D014815">Vitamins</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="Cites"><RefSource>Am J Med Genet. 1999 Nov 19;87(2):168-74</RefSource><PMID Version="1">10533031</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Med Genet. 2000 Jan;37(1):1-8</RefSource><PMID Version="1">10633128</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hum Genet. 2000 Jan;106(1):86-92</RefSource><PMID Version="1">10982187</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Free Radic Res. 2002 Apr;36(4):461-6</RefSource><PMID Version="1">12069111</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Acta Neurol Scand. 2004 Jan;109(1):75-8</RefSource><PMID Version="1">14653855</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Biofactors. 2003;18(1-4):163-71</RefSource><PMID Version="1">14695932</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Can J Neurol Sci. 1976 Nov;3(4):279-86</RefSource><PMID Version="1">1087179</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 1981 Sep;104(3):589-620</RefSource><PMID Version="1">7272714</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 1996 Mar 8;271(5254):1423-7</RefSource><PMID Version="1">8596916</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Am J Hum Genet. 1996 Sep;59(3):554-60</RefSource><PMID Version="1">8751856</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>N Engl J Med. 1996 Oct 17;335(16):1169-75</RefSource><PMID Version="1">8815938</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 1997 Apr;120 ( Pt 4):673-80</RefSource><PMID Version="1">9153129</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Science. 1997 Jun 13;276(5319):1709-12</RefSource><PMID Version="1">9180083</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Nat Genet. 1997 Oct;17(2):215-7</RefSource><PMID Version="1">9326946</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Hum Mol Genet. 1997 Oct;6(11):1771-80</RefSource><PMID Version="1">9302253</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 1997 Dec;120 ( Pt 12):2131-40</RefSource><PMID Version="1">9448568</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurol. 1998 Mar;245(3):166-8</RefSource><PMID Version="1">9553847</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Brain. 1998 Apr;121 ( Pt 4):589-600</RefSource><PMID Version="1">9577387</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Ann Neurol. 1999 Feb;45(2):200-6</RefSource><PMID Version="1">9989622</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Lancet. 1999 Aug 7;354(9177):477-9</RefSource><PMID Version="1">10465173</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurol Sci. 2005 Jun 15;233(1-2):145-62</RefSource><PMID Version="1">15896810</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Arch Neurol. 2007 Apr;64(4):558-64</RefSource><PMID Version="1">17420319</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>J Neurol Sci. 2008 Apr 15;267(1-2):174-6</RefSource><PMID Version="1">17988688</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000293">Adolescent</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000328">Adult</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009202">Cardiomyopathies</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002648">Child</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002675">Child, Preschool</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D016001">Confidence Intervals</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D019587">Dietary Supplements</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D018450">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005621">Friedreich Ataxia</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000150">complications</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000235">genetics</QualifierName><QualifierName MajorTopicYN="N" UI="Q000628">therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007406">Interview, Psychological</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008562">Membrane Glycoproteins</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000235">genetics</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D015999">Multivariate Analysis</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011237">Predictive Value of Tests</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012307">Risk Factors</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012600">Scoliosis</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000209">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014815">Vitamins</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000008">administration & dosage</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D055815">Young Adult</DescriptorName></MeshHeading></MeshHeadingList><OtherID Source="NLM">NIHMS65706</OtherID><OtherID Source="NLM">PMC2579318</OtherID></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>9</Month><Day>2</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>4</Month><Day>9</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>9</Month><Day>2</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.22248</ArticleId><ArticleId IdType="pubmed">18759347</ArticleId><ArticleId IdType="pmc">PMC2579318</ArticleId><ArticleId IdType="mid">NIHMS65706</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Di Prospero, Nicholas A" sort="Di Prospero, Nicholas A" uniqKey="Di Prospero N" first="Nicholas A" last="Di Prospero">Nicholas A. Di Prospero</name><name sortKey="Grow, Chelsea" sort="Grow, Chelsea" uniqKey="Grow C" first="Chelsea" last="Grow">Chelsea Grow</name><name sortKey="Jeffries, Neal" sort="Jeffries, Neal" uniqKey="Jeffries N" first="Neal" last="Jeffries">Neal Jeffries</name><name sortKey="Ravina, Bernard" sort="Ravina, Bernard" uniqKey="Ravina B" first="Bernard" last="Ravina">Bernard Ravina</name></noCountry><country name="États-Unis"><noRegion><name sortKey="La Pean, Alison" sort="La Pean, Alison" uniqKey="La Pean A" first="Alison" last="La Pean">Alison La Pean</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/PubMed/Checkpoint
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002129 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd -nk 002129 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= PubMed
|étape= Checkpoint
|type= RBID
|clé= pubmed:18759347
|texte= Predictors of progression in patients with Friedreich ataxia.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/PubMed/Checkpoint/RBID.i -Sk "pubmed:18759347" \
| HfdSelect -Kh $EXPLOR_AREA/Data/PubMed/Checkpoint/biblio.hfd \
| NlmPubMed2Wicri -a MovDisordV3
| This area was generated with Dilib version V0.6.23. |  |