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Role of the Glyoxalase System in Alzheimer's Disease.
J Alzheimers Dis. 2018; 66(3):887-899.JA

Abstract

Alzheimer's disease (AD) is an insidious and progressive neurodegenerative disease. The main pathological features of AD are the formation of amyloid-β deposits in the anterior cerebral cortex and hippocampus as well as the formation of intracellular neurofibrillary tangles. Thus far, accumulating evidence shows that glycation is closely related to AD. As a final product resulting from the crosslinking of a reducing sugar or other reactive carbonyls and a protein, the advanced glycation end products have been found to be associated with the formation of amyloid-β and neurofibrillary tangles in AD. As a saccharification inhibitor, the glyoxalase system and its substrate methylglyoxal (MG) were certified to be associated with AD onset and development. As an active substance of AGEs, MG could cause direct or indirect damage to nerve cells and tissues. MG is converted to D-lactic acid after decomposition by the glyoxalase system. Under normal circumstances, MG metabolism is in a dynamic equilibrium, whereas MG accumulates in cells in the case of aging or pathological states. Studies have shown that increasing glyoxalase activity and reducing the MG level can inhibit the generation of oxidative stress and AGEs, thereby alleviating the symptoms and signs of AD to some extent. This paper focuses on the relevant mechanisms of action of the glyoxalase system and MG in the pathogenesis of AD, as well as the potential of inhibiting the production of advanced glycation end products in the treatment of AD.

Authors+Show Affiliations

Department of Neurology, Stem Cell Research and Clinical Translation Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.Department of Neurology, Stem Cell Research and Clinical Translation Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.Department of Neurosurgery, Jiangxi Medical College of Nanchang University, Nanchang, Jiangxi, China.Department of Neurology and Stroke Center, the First Affiliated Hospital, Jinan University, Guangzhou, China.Department of Neurology, Stem Cell Research and Clinical Translation Center, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.Department of Neurology, Chongqing General Hospital, University of Chinese Academy of Sciences, Chongqing, People's Republic of China.Institute of Neurology, Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China; Clinical Neuroscience Institute of Jinan University, Guangzhou, China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

30400091

Citation

Jiang, Lianying, et al. "Role of the Glyoxalase System in Alzheimer's Disease." Journal of Alzheimer's Disease : JAD, vol. 66, no. 3, 2018, pp. 887-899.
Jiang L, Wang J, Wang Z, et al. Role of the Glyoxalase System in Alzheimer's Disease. J Alzheimers Dis. 2018;66(3):887-899.
Jiang, L., Wang, J., Wang, Z., Huang, W., Yang, Y., Cai, Z., & Li, K. (2018). Role of the Glyoxalase System in Alzheimer's Disease. Journal of Alzheimer's Disease : JAD, 66(3), 887-899. https://doi.org/10.3233/JAD-180413
Jiang L, et al. Role of the Glyoxalase System in Alzheimer's Disease. J Alzheimers Dis. 2018;66(3):887-899. PubMed PMID: 30400091.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of the Glyoxalase System in Alzheimer's Disease. AU - Jiang,Lianying, AU - Wang,Jiafeng, AU - Wang,Zhigang, AU - Huang,Wenhui, AU - Yang,Yixia, AU - Cai,Zhiyou, AU - Li,Keshen, PY - 2018/11/8/pubmed PY - 2019/11/15/medline PY - 2018/11/8/entrez KW - Advanced glycation end product KW - Alzheimer’s disease KW - glutathione KW - glyoxalase system KW - methylglyoxal SP - 887 EP - 899 JF - Journal of Alzheimer's disease : JAD JO - J Alzheimers Dis VL - 66 IS - 3 N2 - Alzheimer's disease (AD) is an insidious and progressive neurodegenerative disease. The main pathological features of AD are the formation of amyloid-β deposits in the anterior cerebral cortex and hippocampus as well as the formation of intracellular neurofibrillary tangles. Thus far, accumulating evidence shows that glycation is closely related to AD. As a final product resulting from the crosslinking of a reducing sugar or other reactive carbonyls and a protein, the advanced glycation end products have been found to be associated with the formation of amyloid-β and neurofibrillary tangles in AD. As a saccharification inhibitor, the glyoxalase system and its substrate methylglyoxal (MG) were certified to be associated with AD onset and development. As an active substance of AGEs, MG could cause direct or indirect damage to nerve cells and tissues. MG is converted to D-lactic acid after decomposition by the glyoxalase system. Under normal circumstances, MG metabolism is in a dynamic equilibrium, whereas MG accumulates in cells in the case of aging or pathological states. Studies have shown that increasing glyoxalase activity and reducing the MG level can inhibit the generation of oxidative stress and AGEs, thereby alleviating the symptoms and signs of AD to some extent. This paper focuses on the relevant mechanisms of action of the glyoxalase system and MG in the pathogenesis of AD, as well as the potential of inhibiting the production of advanced glycation end products in the treatment of AD. SN - 1875-8908 UR - https://www.unboundmedicine.com/medline/citation/30400091/Role_of_the_Glyoxalase_System_in_Alzheimer's_Disease_ DB - PRIME DP - Unbound Medicine ER -