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|Title: ||Methylglyoxal-Derived Advanced Glycation Endproducts in Multiple Sclerosis|
|Authors: ||Wetzels, Suzan|
Schalkwijk, Casper G.
Hendriks, Jerome J. A.
|Issue Date: ||2017|
|Citation: ||INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 18(2), p. 1-15 (Art N° 421)|
|Abstract: ||Multiple sclerosis (MS) is a demyelinating disease of the central nervous system (CNS). The activation of inflammatory cells is crucial for the development of MS and is shown to induce intracellular glycolytic metabolism in pro-inflammatory microglia and macrophages, as well as
CNS-resident astrocytes. Advanced glycation endproducts (AGEs) are stable endproducts formed by a reaction of the dicarbonyl compounds methylglyoxal (MGO) and glyoxal (GO) with amino acids in proteins, during glycolysis. This suggests that, in MS, MGO-derived AGEs are formed in
glycolysis-driven cells. MGO and MGO-derived AGEs can further activate inflammatory cells by binding to the receptor for advanced glycation endproducts (RAGE). Recent studies have revealed that AGEs are increased in the plasma and brain of MS patients. Therefore, AGEs might contribute to the inflammatory status in MS. Moreover, the main detoxification system of dicarbonyl compounds, the glyoxalase system, seems to be affected in MS patients, which may contribute to high MGO-derived AGE levels. Altogether, evidence is emerging for a contributing role of AGEs
in the pathology of MS. In this review, we provide an overview of the current knowledge on the involvement of AGEs in MS.|
|ISI #: ||000395457700189|
|Type: ||Journal Contribution|
|Appears in Collections: ||Research publications|
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