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Association between white matter hyperintensities and executive decline in mild cognitive impairment is network dependent.

TitleAssociation between white matter hyperintensities and executive decline in mild cognitive impairment is network dependent.
Publication TypeJournal Article
Year of Publication2012
AuthorsJacobs, H. I. L., Visser P. Jelle, Van Boxtel M. P. J., Frisoni G. B., Tsolaki M., Papapostolou P., Nobili F., Wahlund L-O., Minthon L., Frölich L., Hampel H., Soininen H., van de Pol L., Scheltens P., Tan F. E. S., Jolles J., & Verhey F. R. J.
JournalNeurobiol Aging
Volume33
Issue1
Pagination201.e1-8
Date Published2012 Jan
ISSN1558-1497
KeywordsAged, Aged, 80 and over, Cerebral Cortex, Executive Function, Female, Humans, Linear Models, Magnetic Resonance Imaging, Male, Middle Aged, Mild Cognitive Impairment, Time Factors
Abstract

White matter hyperintensities (WMH) in Mild Cognitive Impairment (MCI) have been associated with impaired executive functioning, although contradictory findings have been reported. The aim of this study was to examine whether WMH location influenced the relation between WMH and executive functioning in MCI participants (55-90 years) in the European multicenter memory-clinic-based DESCRIPA study, who underwent MRI scanning at baseline (N = 337). Linear mixed model analysis was performed to test the association between WMH damage in three networks (frontal-parietal, frontal-subcortical and frontal-parietal-subcortical network) and change in executive functioning over a 3-year period. WMH in the frontal-parietal and in the frontal-parietal-subcortical network were associated with decline in executive functioning. However, the frontal-subcortical network was not associated with change in executive functioning. Our results suggest that parietal WMH are a significant contributor to executive decline in MCI and that investigation of WMH in the cerebral networks supporting cognitive functions provide a new way to differentiate stable from cognitive declining MCI individuals.

DOI10.1016/j.neurobiolaging.2010.07.015
Alternate JournalNeurobiol. Aging
PubMed ID20739101

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