한빛사논문
- 조회303
한양대학교 명지병원
Seunghoon Lee, MD, PhD1; Min Soo Byun, MD, PhD2,3; Dahyun Yi, PhD4; Hyejin Ahn, MA5; Gijung Jung, PhD4; Joon Hyung Jung, MD6; Yoon Young Chang, MD, MS7; Kyungtae Kim, MD, MS2; Hyeji Choi, MD, MS2; Jeongmin Choi, MD2; Jun-Young Lee, MD, PhD8; Koung Mi Kang, MD, PhD9; Chul-Ho Sohn, MD, PhD9; Yun-Sang Lee, MD, PhD10; Yu Kyeong Kim, MD, PhD11; Dong Young Lee, MD, PhD2,3,4,5; for the Korean Brain Aging Study for Early Diagnosis and Prediction of Alzheimer Disease (KBASE) Research Group
1Department of Psychiatry, Myongji Hospital, Hanyang University College of Medicine, Goyang, Republic of Korea
2Department of Neuropsychiatry, Seoul National University Hospital, Seoul, Republic of Korea
3Department of Psychiatry, Seoul National University College of Medicine, Seoul, Republic of Korea
4Institute of Human Behavioral Medicine, Medical Research Center, Seoul National University, Seoul, Republic of Korea
5Interdisciplinary Program of Cognitive Science, Seoul National University College of Humanities, Seoul, Republic of Korea
6Department of Psychiatry, Chungbuk National University Hospital, Cheongju, Republic of Korea
7Department of Psychiatry, Inje University, Sanggye Paik Hospital, Seoul, Republic of Korea
8Department of Neuropsychiatry, SMG-SNU Boramae Medical Center, Seoul, Republic of Korea
9Department of Radiology, Seoul National University Hospital, Seoul, Republic of Korea
10Department of Nuclear Medicine, Seoul National University College of Medicine, Seoul, Republic of Korea
11Department of Nuclear Medicine, SMG-SNU Boramae Medical Center, Seoul, Republic of Korea
Corresponding Author: Dong Young Lee, MD, PhD
Abstract
Importance: Many epidemiologic studies have suggested that low levels of plasma leptin, a major adipokine, are associated with increased risk of Alzheimer disease (AD) dementia and cognitive decline. Nevertheless, the mechanistic pathway linking plasma leptin and AD-related cognitive decline is not yet fully understood.
Objective: To examine the association of plasma leptin levels with in vivo AD pathologies, including amyloid-beta (Aβ) and tau deposition, through both cross-sectional and longitudinal approaches among cognitively unimpaired older adults.
Design, setting, and participants: This was a longitudinal cohort study from the Korean Brain Aging Study for Early Diagnosis and Prediction of Alzheimer Disease. Data were collected from January 1, 2014, to December 31, 2020, and data were analyzed from July 11 to September 6, 2022. The study included a total of 208 cognitively unimpaired participants who underwent baseline positron emission tomography (PET) scans for brain Aβ deposition. For longitudinal analyses, 192 participants who completed both baseline and 2-year follow-up PET scans for brain Aβ deposition were included.
Exposure: Plasma leptin levels as assessed by enzyme-linked immunosorbent assay.
Main outcomes and measures: Baseline levels and longitudinal changes of global Aβ and AD-signature region tau deposition measured by PET scans.
Results: Among the 208 participants, the mean (SD) age was 66.0 (11.3) years, 114 were women (54.8%), and 37 were apolipoprotein E ε4 carriers (17.8%). Lower plasma leptin levels had a significant cross-sectional association with greater brain Aβ deposition (β = -0.04; 95% CI, -0.09 to 0.00; P = .046), while there was no significant association between plasma leptin levels and tau deposition (β = -0.02; 95% CI, -0.05 to 0.02; P = .41). In contrast, longitudinal analyses revealed that there was a significant association between lower baseline leptin levels and greater increase of tau deposition over 2 years (β = -0.06; 95% CI, -0.11 to -0.01; P = .03), whereas plasma leptin levels did not have a significant association with longitudinal change of Aβ deposition (β = 0.006; 95% CI, 0.00-0.02; P = .27).
Conclusions and relevance: The present findings suggest that plasma leptin may be protective for the development or progression of AD pathology, including both Aβ and tau deposition.
논문정보
- Research article
- 2024년 05월 (BRIC 등록일 2024-05-07)
- 국내 연구진
- 의약학 > 신경의학
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