scholarly journals TTP4000, a soluble fusion protein inhibitor of Receptor for Advanced Glycation End Products (RAGE) is an effective therapy in animal models of Alzheimer's disease

2013 ◽  
Vol 27 (S1) ◽  
Author(s):  
Bin Zhou ◽  
Robert Rothlein ◽  
Jane Shen ◽  
Carmen Valcarce ◽  
Johan Selmer ◽  
...  
2021 ◽  
pp. 1-11
Author(s):  
Mohamed Haddad ◽  
Morgane Perrotte ◽  
Mohamed Raâfet Ben Khedher ◽  
Elise Madec ◽  
Aurelie Lepage ◽  
...  

Background: Growing evidence supports that receptor for advanced glycation end products (RAGE) and glyoxalase-1 (GLO-1) are implicated in the pathophysiology of Alzheimer’s disease (AD). Extracellular vesicles (EVs) are nanovesicles secreted by almost all cell types, contribute to cellular communication, and are implicated in AD pathology. Recently, EVs are considered as promising tools to identify reliable biomarkers in AD. Objective: The aim of our study was to determine the levels of RAGE and GLO-1 in circulating EVs from mild cognitive impairment (MCI) and AD patients and to analyze their correlation with the clinical Mini-Mental State Examination and Montreal Cognitive Assessment scores. We have studied the possibility that neuronal cells could release and transfer GLO-1 through EVs. Methods: RAGE and GLO-1 levels were measured in circulating EVs, respectively, by Luminex assay and western blot. Released-EVs from SK-N-SH neuronal cells were isolated and GLO-1 levels were determined by western bot. Results: Our data showed higher levels of RAGE in EVs from late AD patients while GLO-1 levels in EVs from early AD were lower as compared to control and MCI patients. Interestingly, levels of RAGE and GLO-1 in EVs were correlated with the cognitive scores regardless of age. For the first time, we demonstrated that GLO-1 was released from neuronal cells through EVs. Conclusion: Although more samples will be needed, our preliminary results support the use of peripheral EVs cargo as new tools for the discovery of peripheral AD biomarkers.


2019 ◽  
Vol 72 (1) ◽  
pp. 191-197 ◽  
Author(s):  
Ping-Song Chou ◽  
Meng-Ni Wu ◽  
Chen-Cheng Yang ◽  
Cheng-Ting Shen ◽  
Yuan-Han Yang

1998 ◽  
Vol 95 (6) ◽  
pp. 555-558 ◽  
Author(s):  
Akinori Takeda ◽  
Takeshi Yasuda ◽  
Toshio Miyata ◽  
Yoji Goto ◽  
Masakazu Wakai ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Kelly N. Z. Fuller ◽  
Edwin R. Miranda ◽  
John P. Thyfault ◽  
Jill K. Morris ◽  
Jacob M. Haus

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.


2009 ◽  
Vol 118 (3) ◽  
pp. 381-389 ◽  
Author(s):  
Michelle Y. Wang ◽  
Fred N. Ross-Cisneros ◽  
Divya Aggarwal ◽  
Chiao-Ying Liang ◽  
Alfredo A. Sadun

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