{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,9]],"date-time":"2026-07-09T06:05:17Z","timestamp":1783577117843,"version":"3.55.0"},"reference-count":76,"publisher":"American Medical Association (AMA)","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Netw Open"],"abstract":"Importance<\/jats:title>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.<\/jats:p><\/jats:sec>Objective<\/jats:title>To examine the association of plasma leptin levels with in vivo AD pathologies, including amyloid-beta (A\u03b2) and tau deposition, through both cross-sectional and longitudinal approaches among cognitively unimpaired older adults.<\/jats:p><\/jats:sec>Design, Setting, and Participants<\/jats:title>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 A\u03b2 deposition. For longitudinal analyses, 192 participants who completed both baseline and 2-year follow-up PET scans for brain A\u03b2 deposition were included.<\/jats:p><\/jats:sec>Exposure<\/jats:title>Plasma leptin levels as assessed by enzyme-linked immunosorbent assay.<\/jats:p><\/jats:sec>Main Outcomes and Measures<\/jats:title>Baseline levels and longitudinal changes of global A\u03b2 and AD-signature region tau deposition measured by PET scans.<\/jats:p><\/jats:sec>Results<\/jats:title>Among the 208 participants, the mean (SD) age was 66.0 (11.3) years, 114 were women (54.8%), and 37 were apolipoprotein E \u03b54 carriers (17.8%). Lower plasma leptin levels had a significant cross-sectional association with greater brain A\u03b2 deposition (\u03b2\u2009=\u2009\u22120.04; 95% CI, \u22120.09 to 0.00; P<\/jats:italic>\u2009=\u2009.046), while there was no significant association between plasma leptin levels and tau deposition (\u03b2\u2009=\u2009\u22120.02; 95% CI, \u22120.05 to 0.02; P<\/jats:italic>\u2009=\u2009.41). 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 (\u03b2\u2009=\u2009\u22120.06; 95% CI, \u22120.11 to \u22120.01; P<\/jats:italic>\u2009=\u2009.03), whereas plasma leptin levels did not have a significant association with longitudinal change of A\u03b2 deposition (\u03b2\u2009=\u20090.006; 95% CI, 0.00-0.02; P<\/jats:italic>\u2009=\u2009.27).<\/jats:p><\/jats:sec>Conclusions and Relevance<\/jats:title>The present findings suggest that plasma leptin may be protective for the development or progression of AD pathology, including both A\u03b2 and tau deposition.<\/jats:p><\/jats:sec>","DOI":"10.1001\/jamanetworkopen.2024.9539","type":"journal-article","created":{"date-parts":[[2024,5,3]],"date-time":"2024-05-03T15:32:41Z","timestamp":1714750361000},"page":"e249539","source":"Crossref","is-referenced-by-count":20,"title":["Plasma Leptin and Alzheimer Protein Pathologies Among Older Adults"],"prefix":"10.1001","volume":"7","author":[{"given":"Seunghoon","family":"Lee","sequence":"first","affiliation":[{"name":"Department of Psychiatry, Myongji Hospital, Hanyang University College of Medicine, Goyang, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Min Soo","family":"Byun","sequence":"additional","affiliation":[{"name":"Department of Neuropsychiatry, Seoul National University Hospital, Seoul, Republic of Korea"},{"name":"Department of Psychiatry, Seoul National University College of Medicine, Seoul, Republic of Korea"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dahyun","family":"Yi","sequence":"additional","affiliation":[{"name":"Institute of Human Behavioral Medicine, Medical Research Center, Seoul National University, Seoul, Republic of 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