Byoung Seok Ye1, Sang Won Seo2, Geon Ha Kim3, Young Noh4, Hanna Cho5, Cindy W Yoon6, Hee Jin Kim7, Juhee Chin7, Seun Jeon8, Jong Min Lee8, Joon-Kyung Seong9, Jae Seung Kim10, Jae-Hong Lee11, Yearn Seong Choe12, Kyung Han Lee12, Young H Sohn13, Michael Ewers14, Michael Weiner15, Duk L Na7. 1. Department of Neurology, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, South Korea; Department of Neurology, Yonsei University College of Medicine, Seoul, South Korea. 2. Department of Neurology, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, South Korea. Electronic address: sangwonseo@empal.com. 3. Department of Neurology, Ewha Womans University School of Medicine, Seoul, South Korea. 4. Department of Neurology, Gachon University Gil Medical Center, Incheon, South Korea. 5. Department of Neurology, Gangnam Severance Hospital, Yonsei University College of Medicine, Seoul, South Korea. 6. Department of Neurology, Inha University School of Medicine, Incheon, South Korea. 7. Department of Neurology, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, South Korea. 8. Department of Biomedical Engineering, Hanyang University, Seoul, South Korea. 9. School of Computer Science and Engineering, Korea University, Seoul, South Korea. 10. Department of Nuclear Medicine, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea. 11. Department of Neurology, University of Ulsan College of Medicine, Asan Medical Center, Seoul, South Korea. 12. Department of Nuclear Medicine, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, South Korea. 13. Department of Neurology, Yonsei University College of Medicine, Seoul, South Korea. 14. Institute for Stroke and Dementia Research, Ludwig-Maximilians-University, Munich, Germany. 15. Department of Veterans Affairs Medical Center, Center for Imaging of Neurodegenerative Diseases, University of California, San Francisco, CA, USA.
Abstract
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.
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 impairedpatients. 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.
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