Altered intracellular signaling and reduced viability of Alzheimer's disease neuronal cybrids is reproduced by β-amyloid peptide acting through receptor for advanced glycation end products (RAGE)

2005 ◽  
Vol 29 (2) ◽  
pp. 333-343 ◽  
Author(s):  
Isaac G. Onyango ◽  
Jeremy B. Tuttle ◽  
James P. Bennett Jr.
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Advanced Glycation End Products ◽  
Intracellular Signaling ◽  
Amyloid Peptide ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Β Amyloid ◽  
Β Amyloid Peptide

Effect of Advanced Glycation End Products on the Progression of Alzheimer’s Disease

2019 ◽  
Vol 72 (1) ◽  
pp. 191-197 ◽  
Author(s):  
Ping-Song Chou ◽  
Meng-Ni Wu ◽  
Chen-Cheng Yang ◽  
Cheng-Ting Shen ◽  
Yuan-Han Yang
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

Advanced glycation end products co-localized with astrocytes and microglial cells in Alzheimer's disease brain

1998 ◽  
Vol 95 (6) ◽  
pp. 555-558 ◽  
Author(s):  
Akinori Takeda ◽  
Takeshi Yasuda ◽  
Toshio Miyata ◽  
Yoji Goto ◽  
Masakazu Wakai ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Advanced Glycation End Products ◽  
Microglial Cells ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

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

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Kelly N. Z. Fuller ◽  
Edwin R. Miranda ◽  
John P. Thyfault ◽  
Jill K. Morris ◽  
Jacob M. Haus
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Advanced Glycation End Products ◽  
Total Serum ◽  
Metabolic Dysfunction ◽  
Advanced Glycation ◽  
Clinical Dementia Rating ◽  
Healthy Elderly ◽  
Glycation End Products ◽  
End Products

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.

scholarly journals Receptor for advanced glycation end products is upregulated in optic neuropathy of Alzheimer’s disease

2009 ◽  
Vol 118 (3) ◽  
pp. 381-389 ◽  
Author(s):  
Michelle Y. Wang ◽  
Fred N. Ross-Cisneros ◽  
Divya Aggarwal ◽  
Chiao-Ying Liang ◽  
Alfredo A. Sadun
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Optic Neuropathy ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products
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