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dc.contributor.authorMcNicoll CF
dc.contributor.authorLatourelle JC
dc.contributor.authorMacDonald ME
dc.contributor.authorLew MF
dc.contributor.authorSuchowersky O
dc.contributor.authorKlein C
dc.contributor.authorGolbe LI
dc.contributor.authorMark MH
dc.contributor.authorGrowdon JH
dc.contributor.authorWooten GF
dc.contributor.authorWatts RL
dc.contributor.authorGuttman M
dc.contributor.authorRacette BA
dc.contributor.authorPerlmutter JS
dc.contributor.authorAhmed A
dc.contributor.authorShill HA
dc.contributor.authorSinger C
dc.contributor.authorSaintHilaire MH
dc.contributor.authorMassood T
dc.contributor.authorHuskey KW
dc.contributor.authorDeStefano AL
dc.contributor.authorGillis T
dc.contributor.authorMysore J
dc.contributor.authorGoldwurm S
dc.contributor.authorPezzoli G
dc.contributor.authorBaker KB
dc.contributor.authorItin I
dc.contributor.authorLitvan I
dc.contributor.authorNicholson G
dc.contributor.authorCorbett A
dc.contributor.authorNance M
dc.contributor.authorDrasby E
dc.contributor.authorIsaacson S
dc.contributor.authorBurn DJ
dc.contributor.authorChinnery PF
dc.contributor.authorPramstaller PP
dc.contributor.authorAl-Hinti J
dc.contributor.authorMoller AT
dc.contributor.authorOstergaard K
dc.contributor.authorSherman SJ
dc.contributor.authorRoxburgh R
dc.contributor.authorSnow B
dc.contributor.authorSlevin JT
dc.contributor.authorCambi F
dc.contributor.authorGusella JF
dc.contributor.authorMyers RH
dc.date.accessioned2018-10-08T09:35:38Z
dc.date.available2018-10-08T09:35:38Z
dc.date.issued2008
dc.identifier.issn0885-3185
dc.identifier.urihttp://dx.doi.org/10.1002/mds.22186
dc.identifier.urihttp://hdl.handle.net/10863/6387
dc.description.abstractThe ATP/ADP ratio reflects mitochondrial function and has been reported to be influenced by the size of the Huntington disease gene (HD) repeat. Impaired mitochondrial function has long been implicated in the pathogenesis of Parkinson's disease (PD), and therefore, we evaluated the relationship of the HD CAG repeat size to PD onset age in a large sample of familial PD cases. PD affected siblings (n = 495), with known onset ages from 248 families, were genotyped for the HD CAG repeat. Genotyping failed in 11 cases leaving 484 for analysis, including 35 LRRK2 carriers. All cases had HD CAG repeats (range, 15-34) below the clinical range for HD, although 5.2% of the sample (n = 25) had repeats in the intermediate range (the intermediate range lower limit = 27; upper limit = 35 repeats), suggesting that the prevalence of intermediate allele carriers in the general population is significant. No relation between the HD CAG repeat size and the age at onset for PD was found in this sample of familial PD.en_US
dc.language.isoenen_US
dc.rights
dc.titleHuntington CAG repeat size does not modify onset age in familial Parkinson's disease: the GenePD studyen_US
dc.typeArticleen_US
dc.date.updated2018-10-08T08:54:19Z
dc.language.isiEN-GB
dc.journal.titleMovement Disorders
dc.description.fulltextnoneen_US


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