ArticleCellular and molecular life sciences : CMLS2011
Alpha-synuclein deficiency leads to increased glyoxalase I expression and glycation stress.
Article in Cellular and molecular life sciences : CMLS, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 90 citations in OpenAlex.
- Targeting Glyoxalase-1 Pathway with Natural Compounds: A Translational Strategy to Reduce Dicarbonyl Stress and Prevent Chronic Diseases.Life (Basel, Switzerland) · 2026Review
- Glycation of alpha-synuclein enhances aggregation and neuroinflammatory responses.NPJ Parkinson's disease · 2025Article
- Proteome-Wide Association Study for Finding Druggable Targets in Progression and Onset of Parkinson's Disease.CNS neuroscience & therapeutics · 2025Article
- A novel function for α-synuclein as a regulator of NCK2 in olfactory bulb: implications for its role in olfaction.Cell & bioscience · 2024Article
- ATM-mediated co-chaperone DNAJB11 phosphorylation facilitates α-synuclein folding upon DNA double-stranded breaks.NAR molecular medicine · 2024Article
- Type 2 Diabetes (T2DM) and Parkinson's Disease (PD): a Mechanistic Approach.Molecular neurobiology · 2023Review
- Advanced glycation end product signaling and metabolic complications: Dietary approach.World journal of diabetes · 2023Review
- RAGE Against the Glycation Machine in Synucleinopathies: Time to Explore New Questions.Journal of Parkinson's disease · 2023Review
- The Glyoxalase System in Age-Related Diseases: Nutritional Intervention as Anti-Ageing Strategy.Cells · 2021Review
- Glyoxalase 1 Expression as a Novel Diagnostic Marker of High-Grade Prostatic Intraepithelial Neoplasia in Prostate Cancer.Cancers · 2021Article
- Yeasts as Complementary Model Systems for the Study of the Pathological Repercussions of Enhanced Synphilin-1 Glycation and Oxidation.International journal of molecular sciences · 2021Article
- Glyoxalase 1 Confers Susceptibility to Schizophrenia: From Genetic Variants to Phenotypes of Neural Function.Frontiers in molecular neuroscience · 2021Article
- The Development of Maillard Reaction, and Advanced Glycation End Product (AGE)-Receptor for AGE (RAGE) Signaling Inhibitors as Novel Therapeutic Strategies for Patients with AGE-Related Diseases.Molecules (Basel, Switzerland) · 2020Review
- Neuroprotection through flavonoid: Enhancement of the glyoxalase pathway.Redox biology · 2018Review
- Comparative Examination of Temporal Glyoxalase 1 Variations Following Perforant Pathway Transection, Excitotoxicity, and Controlled Cortical Impact Injury.Neurotoxicity research · 2018Article
- Linking Glycation and Glycosylation With Inflammation and Mitochondrial Dysfunction in Parkinson's Disease.Frontiers in neuroscience · 2018Review
- Alpha-Synuclein Glycation and the Action of Anti-Diabetic Agents in Parkinson's Disease.Journal of Parkinson's disease · 2018Review
- Probing Protein Glycation by Chromatography and Mass Spectrometry: Analysis of Glycation Adducts.International journal of molecular sciences · 2017Review
- Flavonoid Enhances the Glyoxalase Pathway in Cerebellar Neurons to Retain Cellular Functions.Scientific reports · 2017Article
- Metabolic Dysfunction in Parkinson's Disease: Bioenergetics, Redox Homeostasis and Central Carbon Metabolism.Brain research bulletin · 2017Review
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The presynaptic protein alpha-synuclein has received much attention because its gain-of-function is associated with Parkinson's disease. However, its physiological function is still poorly understood. We studied brain regions of knock-out mice at different ages with regard to consistent upregulations of the transcriptome and focused on glyoxalase I (GLO1). The microarray data were confirmed in qPCR, immunoblot, enzyme activity, and behavior analyses. GLO1 induction is a known protective cellular response to glucose stress, representing efforts to decrease toxic levels of methylglyoxal (MG), glyoxal and advanced glycation endproducts (AGEs). Mass spectrometry quantification demonstrated a ubiquitous increase in MG and fructosyl-lysine as consequences of glucose toxicity, and consistent enhancement of certain AGEs. Thus, GLO1 induction in KO brain seems insufficient to prevent AGE formation. In conclusion, the data demonstrate GLO1 expression and glycation damage to be induced by alpha-synuclein ablation. We propose that wild-type alpha-synuclein modulates brain glucose metabolism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.