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dc.contributor.authorSzvetko, AL
dc.contributor.authorFowdar, J
dc.contributor.authorNelson, J
dc.contributor.authorColson, N
dc.contributor.authorTajouri, L
dc.contributor.authorCsurhes, PA
dc.contributor.authorPender, MP
dc.contributor.authorGriffiths, LR
dc.contributor.editorJournal of the Neurological Sciences
dc.date.accessioned2018-03-22T05:31:57Z
dc.date.available2018-03-22T05:31:57Z
dc.date.issued2007
dc.date.modified2010-01-07T06:44:25Z
dc.identifier.issn0022-510X
dc.identifier.doi10.1016/j.jns.2006.10.006
dc.identifier.urihttp://hdl.handle.net/10072/17777
dc.description.abstractMultiple sclerosis (MS) is a complex neurological disease that affects the central nervous system (CNS) resulting in debilitating neuropathology. Pathogenesis is primarily defined by CNS inflammation and demyelination of nerve axons. Methionine synthase reductase (MTRR) is an enzyme that catalyzes the remethylation of homocysteine (Hcy) to methionine via cobalamin and folate dependant reactions. Cobalamin acts as an intermediate methyl carrier between methylenetetrahydrofolate reductase (MTHFR) and Hcy. MTRR plays a critical role in maintaining cobalamin in an active form and is consequently an important determinant of total plasma Hcy (pHcy) concentrations. Elevated intracellular pHcy levels have been suggested to play a role in CNS dysfunction, neurodegenerative, and cerebrovascular diseases. Our investigation entailed the genotyping of a cohort of 140 cases and matched controls for MTRR and MTHFR, by restriction length polymorphism (RFLP) techniques. Two polymorphisms: MTRR A66G and MTHFR A1298C were investigated in an Australian age and gender matched case-control study. No significant allelic frequency difference was observed between cases and controls at the alpha=0.05 level (MTRR chi(2)=0.005, P=0.95, MTHFR chi(2)=1.15, P=0.28). Our preliminary findings suggest no association between the MTRR A66G and MTHFR A1298C polymorphisms and MS.
dc.description.peerreviewedYes
dc.description.publicationstatusYes
dc.languageEnglish
dc.language.isoeng
dc.publisherJournal of the Neurological Sciences
dc.publisher.placeThe Netherlands
dc.relation.ispartofstudentpublicationN
dc.relation.ispartofpagefrom49
dc.relation.ispartofpageto52
dc.relation.ispartofissue1
dc.relation.ispartofjournalJournal of the Neurological Sciences
dc.relation.ispartofvolume252
dc.rights.retentionY
dc.subject.fieldofresearchClinical sciences
dc.subject.fieldofresearchNeurosciences
dc.subject.fieldofresearchcode3202
dc.subject.fieldofresearchcode3209
dc.titleNo association between MTHFR A1298C and MTRR A66G polymorphisms, and MS in an Australian cohort
dc.typeJournal article
dc.type.descriptionC1 - Articles
dc.type.codeC - Journal Articles
dcterms.licensehttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.description.versionAccepted Manuscript (AM)
gro.facultyGriffith Health, School of Medical Science
gro.rights.copyright© 2007 Elsevier. Licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International Licence (http://creativecommons.org/licenses/by-nc-nd/4.0/) which permits unrestricted, non-commercial use, distribution and reproduction in any medium, providing that the work is properly cited.
gro.date.issued2007
gro.hasfulltextFull Text
gro.griffith.authorColson, Natalie J.


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