Amyloid burden, cerebrovascular disease, brain atrophy, and cognition in cognitively impaired patients

Byoung Seok Ye; Sang Won Seo; Geon Ha Kim; Young Noh; Hanna Cho; Cindy W. Yoon; Hee Jin Kim; Juhee Chin; Seun Jeon; Jong Min Lee; Joon Kyung Seong; Jae Seung Kim; Jae Hong Lee; Yearn Seong Choe; Kyung Han Lee; Young H. Sohn; Michael Ewers; Michael Weiner; Duk L. Na

doi:10.1016/j.jalz.2014.04.521

Amyloid burden, cerebrovascular disease, brain atrophy, and cognition in cognitively impaired patients

Byoung Seok Ye, Sang Won Seo, Geon Ha Kim, Young Noh, Hanna Cho, Cindy W. Yoon, Hee Jin Kim, Juhee Chin, Seun Jeon, Jong Min Lee, Joon Kyung Seong, Jae Seung Kim, Jae Hong Lee, Yearn Seong Choe, Kyung Han Lee, Young H. Sohn, Michael Ewers, Michael Weiner, Duk L. Na

Department of Neurology

Research output: Contribution to journal › Article › peer-review

50 Scopus citations

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.

Original language	English
Pages (from-to)	494-503.e3
Journal	Alzheimer's and Dementia
Volume	11
Issue number	5
DOIs	https://doi.org/10.1016/j.jalz.2014.04.521
State	Published - 1 May 2015

Keywords

Amyloid
Atrophy
Cerebrovascular disease
Cognition
Cortical thickness
Hippocampus
Path analysis
Pittsburgh compound B

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10.1016/j.jalz.2014.04.521

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Ye, B. S., Seo, S. W., Kim, G. H., Noh, Y., Cho, H., Yoon, C. W., Kim, H. J., Chin, J., Jeon, S., Lee, J. M., Seong, J. K., Kim, J. S., Lee, J. H., Choe, Y. S., Lee, K. H., Sohn, Y. H., Ewers, M., Weiner, M., & Na, D. L. (2015). Amyloid burden, cerebrovascular disease, brain atrophy, and cognition in cognitively impaired patients. Alzheimer's and Dementia, 11(5), 494-503.e3. https://doi.org/10.1016/j.jalz.2014.04.521

@article{1b14918264394379992e18a2c60df92a,

title = "Amyloid burden, cerebrovascular disease, brain atrophy, and cognition in cognitively impaired patients",

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.",

keywords = "Amyloid, Atrophy, Cerebrovascular disease, Cognition, Cortical thickness, Hippocampus, Path analysis, Pittsburgh compound B",

author = "Ye, {Byoung Seok} and Seo, {Sang Won} and Kim, {Geon Ha} and Young Noh and Hanna Cho and Yoon, {Cindy W.} and Kim, {Hee Jin} and Juhee Chin and Seun Jeon and Lee, {Jong Min} and Seong, {Joon Kyung} and Kim, {Jae Seung} and Lee, {Jae Hong} and Choe, {Yearn Seong} and Lee, {Kyung Han} and Sohn, {Young H.} and Michael Ewers and Michael Weiner and Na, {Duk L.}",

note = "Funding Information: The authors would like to thank Victoria Barney for English correction. The authors also want to give special thanks to Changsoo Kim for his statistical advice. This study was supported by Basic Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education ( NRF-2013R1A1A2065365 ), the Korean Healthcare Technology R&D Project Ministry for Health & Welfare Affairs ( HI10C2020 & HIC120713 ), the KOSEF NRL program grant (MEST; 2011-0028333 ), Samsung Medical Center ( CRL-108011 & CRS110-14-1 ), and the Converging Research Center Program through the Ministry of Science, ICT and Future Planning, Korea ( 2013K000338 ). Publisher Copyright: {\textcopyright} 2015 The Alzheimer's Association.",

year = "2015",

month = may,

day = "1",

doi = "10.1016/j.jalz.2014.04.521",

language = "English",

volume = "11",

pages = "494--503.e3",

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Ye, BS, Seo, SW, Kim, GH, Noh, Y, Cho, H, Yoon, CW, Kim, HJ, Chin, J, Jeon, S, Lee, JM, Seong, JK, Kim, JS, Lee, JH, Choe, YS, Lee, KH, Sohn, YH, Ewers, M, Weiner, M & Na, DL 2015, 'Amyloid burden, cerebrovascular disease, brain atrophy, and cognition in cognitively impaired patients', Alzheimer's and Dementia, vol. 11, no. 5, pp. 494-503.e3. https://doi.org/10.1016/j.jalz.2014.04.521

TY - JOUR

T1 - Amyloid burden, cerebrovascular disease, brain atrophy, and cognition in cognitively impaired patients

AU - Ye, Byoung Seok

AU - Seo, Sang Won

AU - Kim, Geon Ha

AU - Noh, Young

AU - Cho, Hanna

AU - Yoon, Cindy W.

AU - Kim, Hee Jin

AU - Chin, Juhee

AU - Jeon, Seun

AU - Lee, Jong Min

AU - Seong, Joon Kyung

AU - Kim, Jae Seung

AU - Lee, Jae Hong

AU - Choe, Yearn Seong

AU - Lee, Kyung Han

AU - Sohn, Young H.

AU - Ewers, Michael

AU - Weiner, Michael

AU - Na, Duk L.

N1 - Funding Information: The authors would like to thank Victoria Barney for English correction. The authors also want to give special thanks to Changsoo Kim for his statistical advice. This study was supported by Basic Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education ( NRF-2013R1A1A2065365 ), the Korean Healthcare Technology R&D Project Ministry for Health & Welfare Affairs ( HI10C2020 & HIC120713 ), the KOSEF NRL program grant (MEST; 2011-0028333 ), Samsung Medical Center ( CRL-108011 & CRS110-14-1 ), and the Converging Research Center Program through the Ministry of Science, ICT and Future Planning, Korea ( 2013K000338 ). Publisher Copyright: © 2015 The Alzheimer's Association.

PY - 2015/5/1

Y1 - 2015/5/1

N2 - 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.

AB - 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.

KW - Amyloid

KW - Atrophy

KW - Cerebrovascular disease

KW - Cognition

KW - Cortical thickness

KW - Hippocampus

KW - Path analysis

KW - Pittsburgh compound B

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U2 - 10.1016/j.jalz.2014.04.521

DO - 10.1016/j.jalz.2014.04.521

M3 - Article

C2 - 25048578

AN - SCOPUS:84929281600

VL - 11

SP - 494-503.e3

JO - Alzheimer's and Dementia

JF - Alzheimer's and Dementia

SN - 1552-5260

IS - 5

ER -

Amyloid burden, cerebrovascular disease, brain atrophy, and cognition in cognitively impaired patients

Abstract

Keywords

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