Format

Send to

Choose Destination
See comment in PubMed Commons below
J Amino Acids. 2011;2011:461216. doi: 10.4061/2011/461216. Epub 2011 Mar 14.

Protein modification by dicarbonyl molecular species in neurodegenerative diseases.

Author information

1
Department of Biological Sciences, Case Western Reserve University, Cleveland, OH 44106, USA.

Abstract

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.

PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Hindawi Publishing Corporation Icon for PubMed Central
    Loading ...
    Support Center