Trajectories of Physiological Brain Aging and Related Factors in People Aged from 20 to over-80
- Authors
- Lee, Jin San; Kim, Seonwoo; Yoo, Heejin; Park, Seongbeom; Jang, Young Kyoung; Kim, Hee Jin; Kim, Ko Woon; Kim, Yeshin; Jang, Hyemin; Park, Key-Chung; Yaffe, Kristine; Yang, Jin-Ju; Lee, Jong Min; Na, Duk L.; Seo, Sang Won
- Issue Date
- Sep-2018
- Publisher
- IOS PRESS
- Keywords
- Alzheimer' s disease; cognitive disorders; dementia; magnetic resonance imaging
- Citation
- JOURNAL OF ALZHEIMERS DISEASE, v.65, no.4, pp.1237 - 1246
- Indexed
- SCIE
SCOPUS
- Journal Title
- JOURNAL OF ALZHEIMERS DISEASE
- Volume
- 65
- Number
- 4
- Start Page
- 1237
- End Page
- 1246
- URI
- https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/149373
- DOI
- 10.3233/JAD-170537
- ISSN
- 1387-2877
- Abstract
- Background/Objective: In this study, we investigated a long-term trajectory of brain aging (from the 20 s to over-80) in cognitively normal (CN) individuals. We further determined whether differences in sex, education years, and apolipoprotein E epsilon 4 status affect age-related cortical thinning. Methods: A total of 2,944 CN individuals who underwent high-resolution (3.0-Tesla) magnetic resonance imaging were included in this study. Cortical thickness was measured using a surface-based method. Multiple linear regression analyses were performed to evaluate age-related cortical thinning and related factors. Results: Compared to those in their 20 s/30 s, participants in their 40 s showed thinning primarily in the medial and lateral frontal and inferior parietal regions, and cortical thinning occurred across most of the cortices with increasing age. Notably, the precuneus, inferior temporal and lateral occipital regions were relatively spared until later in life. Male and lower education years were associated with greater cortical thinning with distinct regional specificity. Conclusion: Our findings provide an important clue to understanding the mechanism of age-related cognitive decline and new strategies for preventing the acceleration of pathological brain aging.
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