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Mediators of Inflammation
Volume 2018, Article ID 2061376, 10 pages
https://doi.org/10.1155/2018/2061376
Research Article

Metabolic Derangements Contribute to Reduced sRAGE Isoforms in Subjects with Alzheimer’s Disease

1Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL, USA
2Department of Molecular & Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USA
3Department of Neurology, University of Kansas Medical Center, Fairway, KS, USA

Correspondence should be addressed to Jacob M. Haus; ude.ciu@jsuah

Received 15 November 2017; Accepted 9 January 2018; Published 22 February 2018

Academic Editor: Hermann Gram

Copyright © 2018 Kelly N. Z. Fuller et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Although there is evidence for metabolic dysfunction and chronic inflammation in Alzheimer’s disease (AD), circulating levels of soluble receptor for advanced glycation end products (sRAGE) and the receptor for advanced glycation end products (RAGE) ligand S100B have not been characterized. sRAGE is an important mediator in disease as it can act as a ligand decoy for RAGE and attenuate downstream inflammatory signaling. Cognitively healthy elderly and AD participants with and without type 2 diabetes () were stratified according to the clinical dementia rating (CDR; 0 = normal cognition (NC); ≥0.5 = AD). Total serum sRAGE, endogenous secretory RAGE (esRAGE), and S100B were assayed via ELISAs, and cleaved RAGE (cRAGE) and the cRAGE : esRAGE ratio were calculated. cRAGE : esRAGE was lower in AD compared to NC (). Metabolic substratifications were used to investigate the factors that influence sRAGE pathology in AD. Stratification by BMI classification, median fat mass, median HOMA-IR, median insulin, and median amylin were all metabolic or anthropometric factors which significantly interacted with sRAGE profiles within AD subjects. There were no significant differences in serum S100B between groups. These characterizations of sRAGE contribute evidence to the link between impaired metabolism and cognitive decline due to AD.