Protein Modification by Dicarbonyl Molecular Species in Neurodegenerative Diseases

Neurodegeneration results from abnormalities in cerebral metabolism and energy balance within neurons, astrocytes, microglia, or microvascular endothelial cells of the blood-brain barrier. In Alzheimer's disease, β-amyloid is considered the primary contributor to neuropathology and neurodegener...

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Main Authors:	Williams, Wesley M., Weinberg, Aaron, Smith, Mark A.
Format:	Online
Language:	English
Published:	SAGE-Hindawi Access to Research 2011
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276062/

id	pubmed-3276062
recordtype	oai_dc
spelling	pubmed-32760622012-02-13 Protein Modification by Dicarbonyl Molecular Species in Neurodegenerative Diseases Williams, Wesley M. Weinberg, Aaron Smith, Mark A. Review Article Neurodegeneration results from abnormalities in cerebral metabolism and energy balance within neurons, astrocytes, microglia, or microvascular endothelial cells of the blood-brain barrier. In Alzheimer's disease, β-amyloid is considered the primary contributor to neuropathology and neurodegeneration. It now is believed that certain systemic diseases, such as diabetes mellitus, can contribute to neurodegeneration through the effects of chronic hyperglycemia/insulin resistance resulting in protein glycation, oxidative stress and inflammation within susceptible brain regions. Here, we present an overview of research focusing on the role of protein glycation, oxidative stress, and inflammation in the neurodegenerative process. Of special interest in this paper is the effect of methylglyoxal (MGO), a cytotoxic byproduct of glucose metabolism, elevated in neurodegenerative disease, and diabetes mellitus, on cerebral protein function and oxidative stress. How MGO interacts with amino acid residues within β-amyloid, and small peptides within the brain, is also discussed in terms of the affect on protein function. SAGE-Hindawi Access to Research 2011 2011-03-14 /pmc/articles/PMC3276062/ /pubmed/22332001 http://dx.doi.org/10.4061/2011/461216 Text en Copyright © 2011 Wesley M. Williams et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Williams, Wesley M. Weinberg, Aaron Smith, Mark A.
spellingShingle	Williams, Wesley M. Weinberg, Aaron Smith, Mark A. Protein Modification by Dicarbonyl Molecular Species in Neurodegenerative Diseases
author_facet	Williams, Wesley M. Weinberg, Aaron Smith, Mark A.
author_sort	Williams, Wesley M.
title	Protein Modification by Dicarbonyl Molecular Species in Neurodegenerative Diseases
title_short	Protein Modification by Dicarbonyl Molecular Species in Neurodegenerative Diseases
title_full	Protein Modification by Dicarbonyl Molecular Species in Neurodegenerative Diseases
title_fullStr	Protein Modification by Dicarbonyl Molecular Species in Neurodegenerative Diseases
title_full_unstemmed	Protein Modification by Dicarbonyl Molecular Species in Neurodegenerative Diseases
title_sort	protein modification by dicarbonyl molecular species in neurodegenerative diseases
description	Neurodegeneration results from abnormalities in cerebral metabolism and energy balance within neurons, astrocytes, microglia, or microvascular endothelial cells of the blood-brain barrier. In Alzheimer's disease, β-amyloid is considered the primary contributor to neuropathology and neurodegeneration. It now is believed that certain systemic diseases, such as diabetes mellitus, can contribute to neurodegeneration through the effects of chronic hyperglycemia/insulin resistance resulting in protein glycation, oxidative stress and inflammation within susceptible brain regions. Here, we present an overview of research focusing on the role of protein glycation, oxidative stress, and inflammation in the neurodegenerative process. Of special interest in this paper is the effect of methylglyoxal (MGO), a cytotoxic byproduct of glucose metabolism, elevated in neurodegenerative disease, and diabetes mellitus, on cerebral protein function and oxidative stress. How MGO interacts with amino acid residues within β-amyloid, and small peptides within the brain, is also discussed in terms of the affect on protein function.
publisher	SAGE-Hindawi Access to Research
publishDate	2011
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3276062/
_version_	1611505095026933760

Protein Modification by Dicarbonyl Molecular Species in Neurodegenerative Diseases

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