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Regional subcortical shape analysis in premanifest Huntington’s disease
dc.contributor.authorTang, Xiaoying
dc.contributor.authorRoss, Christopher A.
dc.contributor.authorJohnson, Hans
dc.contributor.authorPaulsen, Jane S.
dc.contributor.authorYounes, Laurent
dc.contributor.authorAlbin, Roger L.
dc.contributor.authorRatnanather, J. Tilak
dc.contributor.authorMiller, Michael I.
dc.date.accessioned2019-03-11T15:35:37Z
dc.date.available2020-06-01T14:50:01Zen
dc.date.issued2019-04-01
dc.identifier.citationTang, Xiaoying; Ross, Christopher A.; Johnson, Hans; Paulsen, Jane S.; Younes, Laurent; Albin, Roger L.; Ratnanather, J. Tilak; Miller, Michael I. (2019). "Regional subcortical shape analysis in premanifest Huntington’s disease." Human Brain Mapping 40(5): 1419-1433.
dc.identifier.issn1065-9471
dc.identifier.issn1097-0193
dc.identifier.urihttps://hdl.handle.net/2027.42/148249
dc.description.abstractHuntington’s disease (HD) involves preferential and progressive degeneration of striatum and other subcortical regions as well as regional cortical atrophy. It is caused by a CAG repeat expansion in the Huntingtin gene, and the longer the expansion the earlier the age of onset. Atrophy begins prior to manifest clinical signs and symptoms, and brain atrophy in premanifest expansion carriers can be studied. We employed a diffeomorphometric pipeline to contrast subcortical structures’ morphological properties in a control group with three disease groups representing different phases of premanifest HD (far, intermediate, and near to onset) as defined by the length of the CAG expansion and the participant’s age (CAG‐Age‐Product). A total of 1,428 magnetic resonance image scans from 694 participants from the PREDICT‐HD cohort were used. We found significant region‐specific atrophies in all subcortical structures studied, with the estimated abnormality onset time varying from structure to structure. Heterogeneous shape abnormalities of caudate nuclei were present in premanifest HD participants estimated furthest from onset and putaminal shape abnormalities were present in participants intermediate to onset. Thalamic, hippocampal, and amygdalar shape abnormalities were present in participants nearest to onset. We assessed whether the estimated progression of subcortical pathology in premanifest HD tracked specific pathways. This is plausible for changes in basal ganglia circuits but probably not for changes in hippocampus and amygdala. The regional shape analyses conducted in this study provide useful insights into the effects of HD pathology in subcortical structures.
dc.publisherJohn Wiley & Sons, Inc.
dc.subject.othersubregion
dc.subject.othersubcortical structures
dc.subject.othershape
dc.subject.otherpremanifest Huntington’s disease
dc.subject.othercircuit
dc.titleRegional subcortical shape analysis in premanifest Huntington’s disease
dc.typeArticle
dc.rights.robotsIndexNoFollow
dc.subject.hlbsecondlevelNeurosciences
dc.subject.hlbsecondlevelKinesiology and Sports
dc.subject.hlbtoplevelHealth Sciences
dc.description.peerreviewedPeer Reviewed
dc.description.bitstreamurlhttps://deepblue.lib.umich.edu/bitstream/2027.42/148249/1/hbm24456.pdf
dc.description.bitstreamurlhttps://deepblue.lib.umich.edu/bitstream/2027.42/148249/2/hbm24456_am.pdf
dc.identifier.doi10.1002/hbm.24456
dc.identifier.sourceHuman Brain Mapping
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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