Journal ArticleDOI
Advanced glycation end-products (AGEs): involvement in aging and in neurodegenerative diseases
TLDR
The mechanism of detoxification of glyoxal and methylglyoxal by the Glyoxalase system is described and also the possibility to eliminate glycated proteins by deglycation enzymes is described.Abstract:
Advanced glycation end-products (AGEs) are formed from the so-called Amadori products by rearrangement followed by other reactions giving rise to compounds bound irreversibly. The structure of some of them is shown and the mechanism of formation is described. Several AGE binding molecules (Receptors for AGE, RAGE) are known and it is thought that many of the effects caused by AGEs are mediated by RAGE. Some of these were shown to be toxic, and called TAGE. The mechanism of detoxification of glyoxal and methylglyoxal by the glyoxalase system is described and also the possibility to eliminate glycated proteins by deglycation enzymes. Compounds able to inhibit AGEs formation are also taken into consideration.read more
Citations
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Journal ArticleDOI
Role of advanced glycation end products in cellular signaling
TL;DR: This review will give an overview of the most prominent AGE-mediated signaling cascades, AGE receptor interactions, prevention of AGE formation and the impact of A GEs during pathophysiological processes.
Journal ArticleDOI
Cellular signalling of the receptor for advanced glycation end products (RAGE).
TL;DR: A comprehensive summary of previous and recent studies relating to the complex molecular network of RAGE signalling, with a particular emphasis on RAGE transgenic mouse models is provided.
Journal ArticleDOI
Methylglyoxal, the dark side of glycolysis
TL;DR: A main emerging concept is that these two neural cell types have different and energetically adapted glyoxalase defense mechanisms which may serve as protective mechanism against methylglyoxal-induced cellular damage.
Journal ArticleDOI
Schiff Bases: A Short Survey on an Evergreen Chemistry Tool
TL;DR: The review reports a short biography of the Italian naturalized chemist Hugo Schiff and an outline on the synthesis and use of his most popular discovery: the imines, very well known and popular as Schiff Bases.
Journal ArticleDOI
Advanced glycation end products and neurodegenerative diseases: Mechanisms and perspective
TL;DR: It is clear that AGEs modification triggers the abnormal deposition and accumulation of the modified proteins, which in turn sustain the local oxidative stress and inflammatory response, eventually leading to the pathological and clinical aspects of neurodegenerative diseases.
References
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Journal ArticleDOI
The multiligand receptor RAGE as a progression factor amplifying immune and inflammatory responses
TL;DR: These features of RAGE allow the receptor to propagate cellular dysfunction in a number of pathophysiologically relevant situations, most often dictated by the formation and persistence of ligands in the tissues.
Journal ArticleDOI
Formation of glyoxal, methylglyoxal and 3-deoxyglucosone in the glycation of proteins by glucose.
TL;DR: Alpha-Oxoaldehydes were formed in early glycation from the degradation of glucose and Schiff's base adduct, which suggests that short periods of hyperglycaemia, as occur in impaired glucose tolerance, may be sufficient to increase the concentrations of alpha-oxoaldeHydes in vivo.
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Glyoxalase I – structure, function and a critical role in the enzymatic defence against glycation
TL;DR: Glyoxalase I has a critical role in the prevention of glycation reactions mediated by methylglyoxal, glyoxal and other alpha-oxoaldehydes in vivo and is particularly important in diabetes and uraemia.
Journal ArticleDOI
Glycated tau protein in alzheimer disease : a mechanism for induction of oxidant stress
Shi Du Yan,Xiao-Tao Chen,Ann Marie Schmidt,J Brett,Gabriel C. Godman,Yu Shan Zou,Clay W Scott,C Caputo,T Frappier,Marie-Louise Smith +9 more
TL;DR: It is proposed that in Alzheimer disease, AGEs in paired helical filament tau can induce oxidant stress, thereby promoting neuronal dysfunction, and being ideal substrates for nonenzymatic glycation.
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Amadorins: novel post-Amadori inhibitors of advanced glycation reactions.
TL;DR: The background and progress that led to discovery of specific inhibition of post-Amadori formation of advanced glycation end products, or AGEs, are focused on, and pyridoxamine (Pyridorin) is identified as the first member of this class of Amadorin compounds.