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Role of Methylglyoxal in Alzheimer's Disease.

Abstract

Alzheimer's disease is the most common and lethal neurodegenerative disorder. The major hallmarks of Alzheimer's disease are extracellular aggregation of amyloid β peptides and, the presence of intracellular neurofibrillary tangles formed by precipitation/aggregation of hyperphosphorylated tau protein. The etiology of Alzheimer's disease is multifactorial and a full understanding of its pathogenesis remains elusive. Some years ago, it has been suggested that glycation may contribute to both extensive protein cross-linking and oxidative stress in Alzheimer's disease. Glycation is an endogenous process that leads to the production of a class of compounds known as advanced glycation end products (AGEs). Interestingly, increased levels of AGEs have been observed in brains of Alzheimer's disease patients. Methylglyoxal, a reactive intermediate of cellular metabolism, is the most potent precursor of AGEs and is strictly correlated with an increase of oxidative stress in Alzheimer's disease. Many studies are showing that methylglyoxal and methylglyoxal-derived AGEs play a key role in the etiopathogenesis of Alzheimer's disease.

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  • Authors

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    Source

    BioMed research international 2014: 2014 pg 238485

    Pub Type(s)

    REVIEW

    Language

    ENG

    PubMed ID

    24734229

    Citation

    TY - JOUR T1 - Role of Methylglyoxal in Alzheimer's Disease. A1 - Angeloni,Cristina, AU - Zambonin,Laura, AU - Hrelia,Silvana, Y1 - 2014/3/9/ PY - 2013/12/13/received PY - 2014/1/28/revised PY - 2014/1/30/accepted PY - 2014/3/9/epublish PY - 2014/4/16/entrez PY - 2014/4/16/pubmed PY - 2014/4/16/medline SP - 238485 EP - 238485 JF - BioMed research international JO - Biomed Res Int VL - 2014 N2 - Alzheimer's disease is the most common and lethal neurodegenerative disorder. The major hallmarks of Alzheimer's disease are extracellular aggregation of amyloid β peptides and, the presence of intracellular neurofibrillary tangles formed by precipitation/aggregation of hyperphosphorylated tau protein. The etiology of Alzheimer's disease is multifactorial and a full understanding of its pathogenesis remains elusive. Some years ago, it has been suggested that glycation may contribute to both extensive protein cross-linking and oxidative stress in Alzheimer's disease. Glycation is an endogenous process that leads to the production of a class of compounds known as advanced glycation end products (AGEs). Interestingly, increased levels of AGEs have been observed in brains of Alzheimer's disease patients. Methylglyoxal, a reactive intermediate of cellular metabolism, is the most potent precursor of AGEs and is strictly correlated with an increase of oxidative stress in Alzheimer's disease. Many studies are showing that methylglyoxal and methylglyoxal-derived AGEs play a key role in the etiopathogenesis of Alzheimer's disease. SN - 2314-6141 UR - https://www.unboundmedicine.com/medline/citation/24734229/full_citation L2 - http://dx.doi.org/10.1155/2014/238485 ER -