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Effects of Alzheimer's and Vascular Pathologies on Structural Connectivity in Early- and Late-Onset Alzheimer's Disease

Authors
Lee, Wha JinYoon, Cindy W.Kim, Sung-WooJeong, Hye JinSeo, SeonghoNa, Duk L.Noh, YoungSeong, Joon-Kyung
Issue Date
16-2월-2021
Publisher
FRONTIERS MEDIA SA
Keywords
early-onset AD; late-onset AD; positron emission tomography; tau; amyloid; small vessel disease; white matter connectivity
Citation
FRONTIERS IN NEUROSCIENCE, v.15
Indexed
SCIE
SCOPUS
Journal Title
FRONTIERS IN NEUROSCIENCE
Volume
15
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/129192
DOI
10.3389/fnins.2021.606600
ISSN
1662-4548
Abstract
Early- and late-onset Alzheimer's disease (AD) patients often exhibit distinct features. We sought to compare overall white matter connectivity and evaluate the pathological factors (amyloid, tau, and vascular pathologies) that affect the disruption of connectivity in these two groups. A total of 50 early- and 38 late-onset AD patients, as well as age-matched cognitively normal participants, were enrolled and underwent diffusion-weighted magnetic resonance imaging to construct fractional anisotropy-weighted white matter connectivity maps. [F-18]-THK5351 PET, [F-18]-Flutemetamol PET, and magnetic resonance imaging were used for the evaluation of tau and related astrogliosis, amyloid, and small vessel disease markers (lacunes and white matter hyperintensities). Cluster-based statistics was performed for connectivity comparisons and correlation analysis between connectivity disruption and the pathological markers. Both patient groups exhibited significantly disrupted connectivity compared to their control counterparts with distinct patterns. Only THK retention was related to connectivity disruption in early-onset AD patients, and this disruption showed correlations with most cognitive scores, while late-onset AD patients had disrupted connectivity correlated with amyloid deposition, white matter hyperintensities, and lacunes in which only a few cognitive scores showed associations. These findings suggest that the pathogenesis of connectivity disruption and its effects on cognition are distinct between EOAD and LOAD.
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