Regional structural hypo‐ and hyperconnectivity of frontal–striatal and frontal–thalamic pathways in behavioral variant frontotemporal dementia
Behavioral variant frontotemporal dementia (bvFTD) has been predominantly considered as a frontotemporal cortical disease, with limited direct investigation of frontal–subcortical connections. We aim to characterize the grey and white matter components of frontal–thalamic and frontal–striatal circui...
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Published in | Human brain mapping Vol. 39; no. 10; pp. 4083 - 4093 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
John Wiley & Sons, Inc
01.10.2018
John Wiley and Sons Inc |
Subjects | |
Online Access | Get full text |
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Summary: | Behavioral variant frontotemporal dementia (bvFTD) has been predominantly considered as a frontotemporal cortical disease, with limited direct investigation of frontal–subcortical connections. We aim to characterize the grey and white matter components of frontal–thalamic and frontal–striatal circuits in bvFTD. Twenty‐four patients with bvFTD and 24 healthy controls underwent morphological and diffusion imaging. Subcortical structures were manually segmented according to published protocols. Probabilistic pathways were reconstructed separately from the dorsolateral, orbitofrontal and medial prefrontal cortex to the striatum and thalamus. Patients with bvFTD had smaller cortical and subcortical volumes, lower fractional anisotropy, and higher mean diffusivity metrics, which is consistent with disruptions in frontal–striatal–thalamic pathways. Unexpectedly, regional volumes of the striatum and thalamus connected to the medial prefrontal cortex were significantly larger in bvFTD (by 135% in the striatum, p = .032, and 217% in the thalamus, p = .004), despite smaller dorsolateral prefrontal cortex connected regional volumes (by 67% in the striatum, p = .002, and 65% in the thalamus, p = .020), and inconsistent changes in orbitofrontal cortex connected regions. These unanticipated findings may represent compensatory or maladaptive remodeling in bvFTD networks. Comparisons are made to other neuropsychiatric disorders suggesting a common mechanism of changes in frontal–subcortical networks; however, longitudinal studies are necessary to test this hypothesis. |
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Bibliography: | Funding information Miller Family Bridgewater Illawarra Health and Medical Research Initiative Summer Scholarship; The Swedish Alzheimer foundation; Thuréus foundation; The Swedish Society for Medical Research; The Bente Rexed Gersteds Foundation for Brain Research Jeffrey C. L. Looi and Alexander F. Santillo contributed equally to this work. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Funding information Miller Family Bridgewater Illawarra Health and Medical Research Initiative Summer Scholarship; The Swedish Alzheimer foundation; Thuréus foundation; The Swedish Society for Medical Research; The Bente Rexed Gersteds Foundation for Brain Research |
ISSN: | 1065-9471 1097-0193 |
DOI: | 10.1002/hbm.24233 |