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dc.contributor.authorTian, Jing
dc.contributor.authorWang, Tienju
dc.contributor.authorJia, Kun
dc.contributor.authorGuo, Lan
dc.contributor.authorSwerdlow, Russell H.
dc.contributor.authorDu, Heng
dc.identifier.citationTian, J., Wang, T., Jia, K., Guo, L., Swerdlow, R. H., & Du, H. (2022). Nonobese Male Patients with Alzheimer's Disease Are Vulnerable to Decrease in Plasma Leptin. Journal of Alzheimer's disease : JAD, 88(3), 1017–1027.
dc.description.abstractBackground:Metabolic dysfunction links to cognitive deficits in Alzheimer’s disease (AD). Leptin is an anti-obesity hormone that modulates energy homeostasis and memory function. Although leptin deregulation is implicated in mouse models of AD-like brain pathology, clinical studies have shown inconsistent results regarding an association of leptin with the development of this neurodegenerative disorder. Objective:We investigated the changes of plasma leptin and the correlation of sex-stratified circulating leptin with cognitive performance, AD-related biological markers, and metabolic status in patients with AD and cognitively unimpaired (CU) counterparts. Methods:We used nonobese AD patients and CU controls in a University of Kansas Medical Center (KUMC) cohort. Plasma leptin levels, circulating AD-related molecules and metabolic profiles were examined and analyzed. Results:In contrast to unchanged circulating leptin in females, male patients exhibited decreased plasma leptin levels compared with male CU counterparts. Moreover, plasma leptin showed no correlation with cognitive performance and AD blood biomarkers in patients with either sex. Of note, females but not males demonstrated an association of plasma leptin with body mass index, high density lipoprotein-cholesterol and its ratio with total cholesterol and triglycerides. Conclusion:Our findings suggest that leptin deficiency is associated with nonobese male AD patients, supporting systemic dysmetabolism in the development of this neurodegenerative disorder in certain populations. Although plasma leptin may have limited capacity to reflect disease severity or progression, future mechanistic studies on the regulation of leptin in nonobese patients with AD would deepen our understanding of the sex-related disparity of AD etiopathogenesis.en_US
dc.publisherIOS Pressen_US
dc.subjectAlzheimer’s diseaseen_US
dc.subjectBlood biomarkeren_US
dc.subjectPlasma leptinen_US
dc.titleNonobese Male Patients with Alzheimer’s Disease Are Vulnerable to Decrease in Plasma Leptinen_US
kusw.kuauthorTian, Jing
kusw.kuauthorWang, Tienju
kusw.kuauthorJia, Kun
kusw.kuauthorGuo, Lan
kusw.kuauthorDu, Heng
kusw.kudepartmentPharmacology and Toxicologyen_US
kusw.kudepartmentHiguchi Biosciences Centeren_US
kusw.oanotesPer Sherpa Romeo 03/02/2023:

Journal of Alzheimer's Disease [Open panel below]Publication Information TitleJournal of Alzheimer's Disease [English] ISSNs Print: 1387-2877 Electronic: 1875-8908 URL PublishersIOS Press [Commercial Publisher] [Open panel below]Publisher Policy Open Access pathways permitted by this journal's policy are listed below by article version. Click on a pathway for a more detailed view.

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NoneCC BYPMC PMC, Journal Website Published Version [pathway c]

NoneCC BY Institutional Repository, Subject Repository, PMC, +1 Accepted Version [pathway a]

None Any Repository, Subject Repository, Funder Designated Location, +3 EmbargoNo Embargo Copyright OwnerAuthors Location Any Repository Author's Homepage Funder Designated Location Institutional Repository Institutional Website Subject Repository Conditions Published sources is acknowledged with citation Must link to published version with DOI Set statement to accompany
kusw.oaversionScholarly/refereed, author accepted manuscripten_US
kusw.oapolicyThis item meets KU Open Access policy criteria.en_US

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