Metabolic Derangements Contribute to Reduced sRAGE Isoforms in Subjects with Alzheimer’s Disease
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...
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Wiley
2018-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2018/2061376 |
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author | Kelly N. Z. Fuller Edwin R. Miranda John P. Thyfault Jill K. Morris Jacob M. Haus |
author_facet | Kelly N. Z. Fuller Edwin R. Miranda John P. Thyfault Jill K. Morris Jacob M. Haus |
author_sort | Kelly N. Z. Fuller |
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description | 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 (n=135) 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 (p<0.05). 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. |
format | Article |
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institution | Kabale University |
issn | 0962-9351 1466-1861 |
language | English |
publishDate | 2018-01-01 |
publisher | Wiley |
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series | Mediators of Inflammation |
spelling | doaj-art-93d84389b27d4547bad7d9521a4f901a2025-02-03T01:24:55ZengWileyMediators of Inflammation0962-93511466-18612018-01-01201810.1155/2018/20613762061376Metabolic Derangements Contribute to Reduced sRAGE Isoforms in Subjects with Alzheimer’s DiseaseKelly N. Z. Fuller0Edwin R. Miranda1John P. Thyfault2Jill K. Morris3Jacob M. Haus4Department of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL, USADepartment of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL, USADepartment of Molecular & Integrative Physiology, University of Kansas Medical Center, Kansas City, KS, USADepartment of Neurology, University of Kansas Medical Center, Fairway, KS, USADepartment of Kinesiology and Nutrition, University of Illinois at Chicago, Chicago, IL, USAAlthough 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 (n=135) 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 (p<0.05). 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.http://dx.doi.org/10.1155/2018/2061376 |
spellingShingle | Kelly N. Z. Fuller Edwin R. Miranda John P. Thyfault Jill K. Morris Jacob M. Haus Metabolic Derangements Contribute to Reduced sRAGE Isoforms in Subjects with Alzheimer’s Disease Mediators of Inflammation |
title | Metabolic Derangements Contribute to Reduced sRAGE Isoforms in Subjects with Alzheimer’s Disease |
title_full | Metabolic Derangements Contribute to Reduced sRAGE Isoforms in Subjects with Alzheimer’s Disease |
title_fullStr | Metabolic Derangements Contribute to Reduced sRAGE Isoforms in Subjects with Alzheimer’s Disease |
title_full_unstemmed | Metabolic Derangements Contribute to Reduced sRAGE Isoforms in Subjects with Alzheimer’s Disease |
title_short | Metabolic Derangements Contribute to Reduced sRAGE Isoforms in Subjects with Alzheimer’s Disease |
title_sort | metabolic derangements contribute to reduced srage isoforms in subjects with alzheimer s disease |
url | http://dx.doi.org/10.1155/2018/2061376 |
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