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JAMA Netw. Open, Mar 03 2025, 8 (3) | https://doi.org/10.1001/jamanetworkopen.2025.0096
Physical Activity, Alzheimer Plasma Biomarkers, and Cognition
Seung Ae Kim, MD1,2; Daeun Shin, MD, MSc3; Hongki Ham, PhD3,4,6,7; Yeshin Kim, MD, PhD8; Yuna Gu, MSc3,5; Hee Jin Kim, MD, PhD3,4,5,6; Duk L. Na, MD, PhD3,9; Henrik Zetterberg, MD10,11,12,13,14,15; Kaj Blennow, MD, PhD10,11,16,17; Sang Won Seo, MD, PhD3,4,5,6,7; Hyemin Jang, MD, PhD1,2; for the Precision Medicine Platform for Mild Cognitive Impairment Based on Multi-omics, Imaging, Evidence-Based R&BD (PREMIER) Consortium
1Department of Neurology, Seoul National University Hospital, Seoul, South Korea
2Seoul National University College of Medicine, Seoul, South Korea
3Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Gangnam-gu, Seoul, South Korea
4Alzheimer’s Disease Convergence Research Center, Samsung Medical Center, Seoul, South Korea
5Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, South Korea
6Department of Digital Health, SAIHST, Sungkyunkwan University, Seoul, South Korea
7Department of Intelligent Precision Healthcare Convergence, Sungkyunkwan University, Suwon, South Korea
8Department of Neurology, Kangwon National University College of Medicine, Chuncheon, South Korea
9Happymid Clinic, Seoul, South Korea
10Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden
11Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Gothenburg, Sweden
12Department of Neurodegenerative Disease, University College London Institute of Neurology, Queen Square, London, United Kingdom
13UK Dementia Research Institute, University College London, London, United Kingdom
14Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China
15Wisconsin Alzheimer’s Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin–Madison, Madison
16Paris Brain Institute, ICM, Pitié-Salpêtrière Hospital, Sorbonne University, Paris, France
17Neurodegenerative Disorder Research Center, Division of Life Sciences and Medicine, and Department of Neurology, Institute on Aging and Brain Disorders, University of Science and Technology of China and First Affiliated Hospital of USTC, Hefei, China
Corresponding Author: Hyemin Jang, MD, PhD
1Department of Neurology, Seoul National University Hospital, Seoul, South Korea
2Seoul National University College of Medicine, Seoul, South Korea
3Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Gangnam-gu, Seoul, South Korea
4Alzheimer’s Disease Convergence Research Center, Samsung Medical Center, Seoul, South Korea
5Department of Health Sciences and Technology, SAIHST, Sungkyunkwan University, Seoul, South Korea
6Department of Digital Health, SAIHST, Sungkyunkwan University, Seoul, South Korea
7Department of Intelligent Precision Healthcare Convergence, Sungkyunkwan University, Suwon, South Korea
8Department of Neurology, Kangwon National University College of Medicine, Chuncheon, South Korea
9Happymid Clinic, Seoul, South Korea
10Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden
11Clinical Neurochemistry Laboratory, Sahlgrenska University Hospital, Gothenburg, Sweden
12Department of Neurodegenerative Disease, University College London Institute of Neurology, Queen Square, London, United Kingdom
13UK Dementia Research Institute, University College London, London, United Kingdom
14Hong Kong Center for Neurodegenerative Diseases, Hong Kong, China
15Wisconsin Alzheimer’s Disease Research Center, University of Wisconsin School of Medicine and Public Health, University of Wisconsin–Madison, Madison
16Paris Brain Institute, ICM, Pitié-Salpêtrière Hospital, Sorbonne University, Paris, France
17Neurodegenerative Disorder Research Center, Division of Life Sciences and Medicine, and Department of Neurology, Institute on Aging and Brain Disorders, University of Science and Technology of China and First Affiliated Hospital of USTC, Hefei, China
Corresponding Author: Hyemin Jang, MD, PhD
Abstract
Importance: Physical activity (PA) is a nonpharmacological intervention for dementia prevention. The association between PA and Alzheimer disease (AD) plasma biomarkers remains underexplored.
Objective: To investigate the associations among PA; plasma biomarkers, including β-amyloid 42/40 (Aβ42/40), phosphorylated-tau217 (ptau217), glial fibrillary acidic protein (GFAP), and neurofilament light chain (NfL); and cognition.
Design, setting, and participants: This cross-sectional study included participants with and without cognitive impairment recruited from multiple memory clinics in South Korea between May 2019 and May 2022. Data were analyzed from June to December 2024.
Exposures: PA was assessed as metabolic equivalent task minutes per week using the International Physical Activity Questionnaire and categorized into quartiles from the lowest (Q1) to the highest (Q4).
Main outcomes and measures: Plasma Aβ42/40, ptau217, GFAP, and NfL were measured. Cognition was assessed using the Mini-Mental State Examination (MMSE) and Clinical Dementia Rating-Sum of Boxes (CDR-SB).
Results: Among 1144 participants (mean [SD] age 70.9 [8.7] years; 744 [65.0%] female), the highest PA quartile showed significantly lower ptau217 (estimate [SE], -0.14 [0.06]; P = .01) and NfL (estimate [SE], -0.12 [0.05]; P = .01) compared with the lowest quartile. Higher PA quartiles were associated with higher MMSE scores (estimate [SE]: Q2, 0.93 [0.31]; P = .003; Q3, 0.82 [0.32]; P = .009; Q4, 0.94 [0.32]; P = .004) and lower CDR-SB scores (estimate [SE]: Q2, -0.33 [0.16]; P = .04; Q3, -0.37 [0.16]; P = .02; Q4, -0.55 [0.16]; P = .001) after adjusting for age, sex, education years, and β-amyloid uptake. In subgroup analyses according to age and cognitive status, the associations of PA and plasma biomarkers with cognition were more pronounced in the older (age ≥65 years) and cognitively impaired groups compared with the younger and cognitively unimpaired groups.
Conclusions and relevance: These findings suggest that PA may help delay cognitive decline by modulating neurodegeneration and AD-specific tau pathologies. However, the cross-sectional design limits causal inference, and longitudinal studies are needed to confirm and clarify these associations.
Objective: To investigate the associations among PA; plasma biomarkers, including β-amyloid 42/40 (Aβ42/40), phosphorylated-tau217 (ptau217), glial fibrillary acidic protein (GFAP), and neurofilament light chain (NfL); and cognition.
Design, setting, and participants: This cross-sectional study included participants with and without cognitive impairment recruited from multiple memory clinics in South Korea between May 2019 and May 2022. Data were analyzed from June to December 2024.
Exposures: PA was assessed as metabolic equivalent task minutes per week using the International Physical Activity Questionnaire and categorized into quartiles from the lowest (Q1) to the highest (Q4).
Main outcomes and measures: Plasma Aβ42/40, ptau217, GFAP, and NfL were measured. Cognition was assessed using the Mini-Mental State Examination (MMSE) and Clinical Dementia Rating-Sum of Boxes (CDR-SB).
Results: Among 1144 participants (mean [SD] age 70.9 [8.7] years; 744 [65.0%] female), the highest PA quartile showed significantly lower ptau217 (estimate [SE], -0.14 [0.06]; P = .01) and NfL (estimate [SE], -0.12 [0.05]; P = .01) compared with the lowest quartile. Higher PA quartiles were associated with higher MMSE scores (estimate [SE]: Q2, 0.93 [0.31]; P = .003; Q3, 0.82 [0.32]; P = .009; Q4, 0.94 [0.32]; P = .004) and lower CDR-SB scores (estimate [SE]: Q2, -0.33 [0.16]; P = .04; Q3, -0.37 [0.16]; P = .02; Q4, -0.55 [0.16]; P = .001) after adjusting for age, sex, education years, and β-amyloid uptake. In subgroup analyses according to age and cognitive status, the associations of PA and plasma biomarkers with cognition were more pronounced in the older (age ≥65 years) and cognitively impaired groups compared with the younger and cognitively unimpaired groups.
Conclusions and relevance: These findings suggest that PA may help delay cognitive decline by modulating neurodegeneration and AD-specific tau pathologies. However, the cross-sectional design limits causal inference, and longitudinal studies are needed to confirm and clarify these associations.
논문정보
- Research article
- 2025년 03월 (BRIC 등록일 2025-03-11)
- 국내(교신)+국외 연구진
- 의약학 > 응용의학
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