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Amyloid burden, cerebrovascular disease, brain atrophy, and cognition in cognitively impaired patients
Author(s) -
Ye Byoung Seok,
Seo Sang Won,
Kim Geon Ha,
Noh Young,
Cho Hanna,
Yoon Cindy W.,
Kim Hee Jin,
Chin Juhee,
Jeon Seun,
Lee Jong Min,
Seong Joon-Kyung,
Kim Jae Seung,
Lee Jae-Hong,
Choe Yearn Seong,
Lee Kyung Han,
Sohn Young H.,
Ewers Michael,
Weiner Michael,
Na Duk L.
Publication year - 2015
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2014.04.521
Subject(s) - atrophy , pittsburgh compound b , hyperintensity , cognition , psychology , neuroscience , hippocampal formation , dementia , effects of sleep deprivation on cognitive performance , episodic memory , alzheimer's disease , cognitive decline , medicine , cardiology , disease , cognitive impairment , magnetic resonance imaging , radiology
Background We investigated the independent effects of Alzheimer's disease (AD) and cerebrovascular disease (CVD) pathologies on brain structural changes and cognition. Methods Amyloid burden (Pittsburgh compound B [PiB] retention ratio), CVD markers (volume of white matter hyperintensities [WMH] and number of lacunae), and structural changes (cortical thickness and hippocampal shape) were measured in 251 cognitively impaired patients. Path analyses were utilized to assess the effects of these markers on cognition. Results PiB retention ratio was associated with hippocampal atrophy, which was associated with memory impairment. WMH were associated with frontal thinning, which was associated with executive and memory dysfunctions. PiB retention ratio and lacunae were also associated with memory and executive dysfunction without the mediation of hippocampal or frontal atrophy. Conclusions Our results suggest that the impacts of AD and CVD pathologies on cognition are mediated by specific brain regions.