Journal ArticleDOI
Proteomics analysis of methylglyoxal-induced neurotoxic effects in SH-SY5Y cells.
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TLDR
The results suggest that multiple pathways are potentially involved in MG‐induced neuron death, including actin, immunoglobulin lambda light chain and protein phosphatase 2, which are noteworthy given their functional roles in AD pathogenesis.Abstract:
Reactive carbonyl compounds contribute to aging, Alzheimer's disease (AD) and other neurodegenerative diseases. Among these compounds, methylglyoxal (MG) can yield advanced glycation end products (AGEs), which are crucial in AD pathogenesis. However, the molecular and biochemical mechanisms of MG neurotoxicity are not completely understood. In the present study, SH-SY5Y cells were treated with MG to induce cell death. 2-D Fluorescence Difference Gel Electrophoresis and matrix-assisted laser desorption/ionization-time of flight mass spectrometry were employed to determine the changes in protein levels in these cells compared with vehicle-treated cells. Proteomics analysis revealed that 49 proteins were differentially expressed in MG-treated SH-SY5Y cells, of which 16 were upregulated and 33 were downregulated. Among them, eight proteins were identified unambiguously. The significant changes in protein levels of actin, immunoglobulin lambda light chain and protein phosphatase 2 were noteworthy given their functional roles in AD pathogenesis. Taken together, our results suggest that multiple pathways are potentially involved in MG-induced neuron death. Copyright © 2010 John Wiley & Sons, Ltd.read more
Citations
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Journal ArticleDOI
Advanced glycation end products and neurodegenerative diseases: Mechanisms and perspective
TL;DR: It is clear that AGEs modification triggers the abnormal deposition and accumulation of the modified proteins, which in turn sustain the local oxidative stress and inflammatory response, eventually leading to the pathological and clinical aspects of neurodegenerative diseases.
Journal ArticleDOI
Glyoxalase 1 increases anxiety by reducing GABAA receptor agonist methylglyoxal
Margaret G. Distler,Leigh D. Plant,Greta Sokoloff,Andrew J. Hawk,Ivy Aneas,Gerald E. Wuenschell,John Termini,Stephen C. Meredith,Marcelo A. Nobrega,Abraham A. Palmer +9 more
TL;DR: The data indicate that GLO1 increases anxiety by reducing levels of MG, thereby decreasing GABAA receptor activation, and potentially link metabolic state, neuronal inhibitory tone, and behavior.
Journal ArticleDOI
Role of Glyoxalase 1 (Glo1) and methylglyoxal (MG) in behavior: recent advances and mechanistic insights
TL;DR: A review highlights GLO1's association with behavioral phenotypes, describes recent discoveries that have elucidated the underlying mechanisms, and identifies opportunities for future research.
Journal ArticleDOI
Energy metabolism, proteotoxic stress and age-related dysfunction - protection by carnosine.
TL;DR: It is proposed that excessive glycolysis, rather than aerobic activity, could be causal to proteotoxic stress and age-related pathology, due to the generation of endogenous glycating metabolites: the deleterious role of methylglyoxal (MG) is emphasized.
Journal ArticleDOI
Glycated proteome: from reaction to intervention.
TL;DR: This review discusses the strategies to characterizeprotein glycation, its functional implications in different diseases, and intervention strategies to protect the deleterious effects of protein glycation.
References
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Protein oxidation in the brain in Alzheimer's disease.
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Journal ArticleDOI
Acrolein is increased in Alzheimer’s disease brain and is toxic to primary hippocampal cultures
TL;DR: It is shown that acrolein is increased in the brain in AD and neurotoxicity mechanisms that might be important in the pathogenesis of neuron degeneration in AD are demonstrated.
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Immunoglobulins and complement factors in senile plaques. An immunoperoxidase study
Piet Eikelenboom,F. C. Stam +1 more
TL;DR: In this paper, the authors used immunoperoxidase techniques to obtain information about the possible presence of serum factors in senile plaques, and they found that only in plaques consisting of an amyloid core surrounded by a corona of degenerating neurites small amounts of IgG and light chains (kappa and labda).
Journal ArticleDOI
4-Hydroxynonenal, a product of lipid peroxidation, inhibits dephosphorylation of the microtubule-associated protein tau.
TL;DR: Following exposure of cultured rat hippocampal neurons to 4-hydroxy-nonenal (HNE), an aldehydic product of membrane lipid peroxidation, tau is resistant to dephoshorylation, and a role for HNE is suggested in altered tau phosphorylation and neurofibrillary degeneration in AD.
Journal ArticleDOI
Actin carbonylation: from a simple marker of protein oxidation to relevant signs of severe functional impairment.
Isabella Dalle-Donne,Ranieri Rossi,Daniela Giustarini,Nicoletta Gagliano,Lorenzo Lusini,Aldo Milzani,P. Di Simplicio,Roberta Colombo +7 more
TL;DR: The increase in actin content of carbonyl groups found in vivo would indicate drastic oxidative modification leading to drastic functional impairments.