Homocysteine is not associated with global motor or cognitive measures in nondemented older Parkinson's disease patients.
Identifieur interne : 000973 ( Ncbi/Merge ); précédent : 000972; suivant : 000974Homocysteine is not associated with global motor or cognitive measures in nondemented older Parkinson's disease patients.
Auteurs : Richard M. Camicioli [Canada] ; Thomas P. Bouchard ; Martin J. SomervilleSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2009.
English descriptors
- KwdEn :
- Aged, Antiparkinson Agents (administration & dosage), Antiparkinson Agents (adverse effects), Antiparkinson Agents (pharmacokinetics), Antiparkinson Agents (therapeutic use), Cognition, Creatinine (blood), Female, Folic Acid (blood), Genotype, Homocysteine (biosynthesis), Homocysteine (blood), Humans, Inactivation, Metabolic, Levodopa (administration & dosage), Levodopa (adverse effects), Levodopa (pharmacokinetics), Levodopa (therapeutic use), Male, Methylation, Methylenetetrahydrofolate Reductase (NADPH2) (genetics), Motor Skills, Neuropsychological Tests, Parkinson Disease (blood), Parkinson Disease (physiopathology), Parkinson Disease (psychology), Severity of Illness Index, Vitamin B Complex (administration & dosage).
- MESH :
- chemical , administration & dosage : Antiparkinson Agents, Levodopa, Vitamin B Complex.
- chemical , adverse effects : Antiparkinson Agents, Levodopa.
- chemical , biosynthesis : Homocysteine.
- chemical , blood : Creatinine, Folic Acid, Homocysteine.
- chemical , genetics : Methylenetetrahydrofolate Reductase (NADPH2).
- chemical , pharmacokinetics : Antiparkinson Agents, Levodopa.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- blood : Parkinson Disease.
- physiopathology : Parkinson Disease.
- psychology : Parkinson Disease.
- Aged, Cognition, Female, Genotype, Humans, Inactivation, Metabolic, Male, Methylation, Motor Skills, Neuropsychological Tests, Severity of Illness Index.
Abstract
Levodopa (L-dopa) treatment of Parkinson's disease (PD) is associated with elevated homocysteine (Hcy). To examine the relationship between Hcy, methylenetetrahydrofolate reductase polymorphisms (MTHFR: 677C/T; 1298A/C), and B-vitamins in older PD patients and whether Hcy or MTHFR polymorphisms were associated with clinical measures. MTHFR polymorphisms, B-vitamin intake, and blood concentrations of Hcy, vitamin B12 and folate, and creatinine were determined and compared between groups (PD and controls). The relationship of Hcy to clinical measures was examined in PD. Among 51 patients [30M/21F, mean age (SD): 71.5 (4.7)] and 50 controls [29M/21F, 71.5 (4.8)], Hcy was higher in PD [13.6 (3.8); controls: 10.5 (2.5), P < 0.0005]. Hcy was associated with B-vitamin intake [F = 21.7, P < 0.0005], folate level (R = 0.31, P = 0.035), and the interaction of intake with MTHFR 677T (F = 5.2, P = 0.007), but not MTHFR 1298C genotype. Hcy did not correlate with global measures of cognition, mood, or parkinsonism in PD or with dyskinesias, fluctuations, or freezing. Higher vitamin B12 levels were associated with lower dyskinesia risk. Hcy was influenced by PD, MTHFR 677 genotype, and vitamin use, but not by the MTHFR 1298 genotype. There was no clear association with motor or cognitive measures, but dyskinesias were less likely with higher B12.
DOI: 10.1002/mds.22227
PubMed: 18951534
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Camicioli</name><affiliation wicri:level="1"><nlm:affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta Canada. rcamicio@ualberta.ca</nlm:affiliation><country wicri:rule="url">Canada</country></affiliation></author><author><name sortKey="Bouchard, Thomas P" sort="Bouchard, Thomas P" uniqKey="Bouchard T" first="Thomas P" last="Bouchard">Thomas P. Bouchard</name></author><author><name sortKey="Somerville, Martin J" sort="Somerville, Martin J" uniqKey="Somerville M" first="Martin J" last="Somerville">Martin J. Somerville</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="2009" type="published">2009</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Antiparkinson Agents (administration & dosage)</term><term>Antiparkinson Agents (adverse effects)</term><term>Antiparkinson Agents (pharmacokinetics)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Cognition</term><term>Creatinine (blood)</term><term>Female</term><term>Folic Acid (blood)</term><term>Genotype</term><term>Homocysteine (biosynthesis)</term><term>Homocysteine (blood)</term><term>Humans</term><term>Inactivation, Metabolic</term><term>Levodopa (administration & dosage)</term><term>Levodopa (adverse effects)</term><term>Levodopa (pharmacokinetics)</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Methylation</term><term>Methylenetetrahydrofolate Reductase (NADPH2) (genetics)</term><term>Motor Skills</term><term>Neuropsychological Tests</term><term>Parkinson Disease (blood)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson Disease (psychology)</term><term>Severity of Illness Index</term><term>Vitamin B Complex (administration & dosage)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term><term>Vitamin B Complex</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Homocysteine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Creatinine</term><term>Folic Acid</term><term>Homocysteine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Methylenetetrahydrofolate Reductase (NADPH2)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacokinetics" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="psychology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Cognition</term><term>Female</term><term>Genotype</term><term>Humans</term><term>Inactivation, Metabolic</term><term>Male</term><term>Methylation</term><term>Motor Skills</term><term>Neuropsychological Tests</term><term>Severity of Illness Index</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Levodopa (L-dopa) treatment of Parkinson's disease (PD) is associated with elevated homocysteine (Hcy). To examine the relationship between Hcy, methylenetetrahydrofolate reductase polymorphisms (MTHFR: 677C/T; 1298A/C), and B-vitamins in older PD patients and whether Hcy or MTHFR polymorphisms were associated with clinical measures. MTHFR polymorphisms, B-vitamin intake, and blood concentrations of Hcy, vitamin B12 and folate, and creatinine were determined and compared between groups (PD and controls). The relationship of Hcy to clinical measures was examined in PD. Among 51 patients [30M/21F, mean age (SD): 71.5 (4.7)] and 50 controls [29M/21F, 71.5 (4.8)], Hcy was higher in PD [13.6 (3.8); controls: 10.5 (2.5), P < 0.0005]. Hcy was associated with B-vitamin intake [F = 21.7, P < 0.0005], folate level (R = 0.31, P = 0.035), and the interaction of intake with MTHFR 677T (F = 5.2, P = 0.007), but not MTHFR 1298C genotype. Hcy did not correlate with global measures of cognition, mood, or parkinsonism in PD or with dyskinesias, fluctuations, or freezing. Higher vitamin B12 levels were associated with lower dyskinesia risk. Hcy was influenced by PD, MTHFR 677 genotype, and vitamin use, but not by the MTHFR 1298 genotype. There was no clear association with motor or cognitive measures, but dyskinesias were less likely with higher B12.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18951534</PMID><DateCreated><Year>2009</Year><Month>02</Month><Day>02</Day></DateCreated><DateCompleted><Year>2009</Year><Month>06</Month><Day>08</Day></DateCompleted><DateRevised><Year>2014</Year><Month>11</Month><Day>20</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>24</Volume><Issue>2</Issue><PubDate><Year>2009</Year><Month>Jan</Month><Day>30</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Homocysteine is not associated with global motor or cognitive measures in nondemented older Parkinson's disease patients.</ArticleTitle><Pagination><MedlinePgn>176-82</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.22227</ELocationID><Abstract><AbstractText>Levodopa (L-dopa) treatment of Parkinson's disease (PD) is associated with elevated homocysteine (Hcy). To examine the relationship between Hcy, methylenetetrahydrofolate reductase polymorphisms (MTHFR: 677C/T; 1298A/C), and B-vitamins in older PD patients and whether Hcy or MTHFR polymorphisms were associated with clinical measures. MTHFR polymorphisms, B-vitamin intake, and blood concentrations of Hcy, vitamin B12 and folate, and creatinine were determined and compared between groups (PD and controls). The relationship of Hcy to clinical measures was examined in PD. Among 51 patients [30M/21F, mean age (SD): 71.5 (4.7)] and 50 controls [29M/21F, 71.5 (4.8)], Hcy was higher in PD [13.6 (3.8); controls: 10.5 (2.5), P < 0.0005]. Hcy was associated with B-vitamin intake [F = 21.7, P < 0.0005], folate level (R = 0.31, P = 0.035), and the interaction of intake with MTHFR 677T (F = 5.2, P = 0.007), but not MTHFR 1298C genotype. Hcy did not correlate with global measures of cognition, mood, or parkinsonism in PD or with dyskinesias, fluctuations, or freezing. Higher vitamin B12 levels were associated with lower dyskinesia risk. Hcy was influenced by PD, MTHFR 677 genotype, and vitamin use, but not by the MTHFR 1298 genotype. There was no clear association with motor or cognitive measures, but dyskinesias were less likely with higher B12.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Camicioli</LastName><ForeName>Richard M</ForeName><Initials>RM</Initials><AffiliationInfo><Affiliation>Department of Medicine (Neurology), University of Alberta, Edmonton, Alberta Canada. rcamicio@ualberta.ca</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bouchard</LastName><ForeName>Thomas P</ForeName><Initials>TP</Initials></Author><Author ValidYN="Y"><LastName>Somerville</LastName><ForeName>Martin J</ForeName><Initials>MJ</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</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="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>0LVT1QZ0BA</RegistryNumber><NameOfSubstance UI="D006710">Homocysteine</NameOfSubstance></Chemical><Chemical><RegistryNumber>12001-76-2</RegistryNumber><NameOfSubstance UI="D014803">Vitamin B Complex</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>935E97BOY8</RegistryNumber><NameOfSubstance UI="D005492">Folic Acid</NameOfSubstance></Chemical><Chemical><RegistryNumber>AYI8EX34EU</RegistryNumber><NameOfSubstance UI="D003404">Creatinine</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.5.1.20</RegistryNumber><NameOfSubstance UI="D042965">Methylenetetrahydrofolate Reductase 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MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000523" MajorTopicYN="N">psychology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012720" MajorTopicYN="N">Severity of Illness Index</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D014803" MajorTopicYN="N">Vitamin B Complex</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>2008</Year><Month>10</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2009</Year><Month>6</Month><Day>9</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2008</Year><Month>10</Month><Day>28</Day><Hour>9</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">18951534</ArticleId><ArticleId IdType="doi">10.1002/mds.22227</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Canada</li></country></list><tree><noCountry><name sortKey="Bouchard, Thomas P" sort="Bouchard, Thomas P" uniqKey="Bouchard T" first="Thomas P" last="Bouchard">Thomas P. Bouchard</name><name sortKey="Somerville, Martin J" sort="Somerville, Martin J" uniqKey="Somerville M" first="Martin J" last="Somerville">Martin J. Somerville</name></noCountry><country name="Canada"><noRegion><name sortKey="Camicioli, Richard M" sort="Camicioli, Richard M" uniqKey="Camicioli R" first="Richard M" last="Camicioli">Richard M. Camicioli</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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