ArticleNeurotoxicity research2022
The Methylglyoxal/RAGE/NOX-2 Pathway is Persistently Activated in the Hippocampus of Rats with STZ-Induced Sporadic Alzheimer's Disease.
Article in Neurotoxicity research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 24 citations in OpenAlex.
- An Integrated Analysis of Manganese Metabolism-Related Genes and Their Association With Biomarkers, Immune Infiltration, and Clinical Subtypes in Alzheimer's Disease.Genes, brain, and behavior · 2026Article
- The Senescent Phenotype of Cultured Hypothalamic Astrocytes from Rats with Streptozotocin-Induced Dementia.Neurochemical research · 2026Article
- Polyphenol-based modulation of the Glo1-Nrf2-RAGE axis in diabetes and neurodegeneration: mechanistic evidence, translational constraints, and critical appraisal.Frontiers in pharmacology · 2026Review
- Fucoxanthin attenuates carbonyl stress and neuroinflammation by modulating MGO/RAGE/NF-κB axis in Aβ-induced models.Frontiers in pharmacology · 2026Article
- A novel perspective on the ameliorating effects of catechin-carbonyl adducts on AGEs toxicity.Current research in food science · 2026Article
- Neuroprotective Roles of Metformin in a Streptozotocin-Induced Dementia Model in Rats.Neurotoxicity research · 2025Article
- Methylglyoxal, a Knot to Be Untied in Brain Glucose Hypometabolism.Metabolites · 2025Review
- The RAGE Inhibitor TTP488 (Azeliragon) Improves Diabetic Bladder Dysfunction in Leptin-Deficient Obese Mice.Antioxidants (Basel, Switzerland) · 2025Article
- Sex-Associated Cerebellar and Hippocampal Volume Reduction in Alzheimer's Disease: Insights from the Clinical ADNI Cohort and STZ Animal Model.International journal of molecular sciences · 2025Article
- Pathological role of RAGE underlying progression of various diseases: its potential as biomarker and therapeutic target.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Methylglyoxal Formation-Metabolic Routes and Consequences.Antioxidants (Basel, Switzerland) · 2025Review
- Lithium Chloride Improves Electrophysiological and Memory Deficits in Rats with Streptozotocin-Induced Alzheimer's Disease.Current Alzheimer research · 2025Article
- Meloxicam mitigated methylglyoxal-induced glycative stress in rats.Iranian journal of basic medical sciences · 2025Article
- Targeting glycolysis for neuroprotection in early LPS-induced neuroinflammation.Brain, behavior, & immunity - health · 2024Article
- Methylglyoxal Affects the Expression of miR-125b, miR-107, and Oxidative Stress Pathway-associated Genes in the SH-SY5Y Cell Line.Advanced pharmaceutical bulletin · 2024Article
- Changes in Astroglial Water Flow in the Pre-amyloid Phase of the STZ Model of AD Dementia.Neurochemical research · 2024Article
- Annao Pingchong decoction attenuates oxidative stress and neuronal apoptosis following intracerebral hemorrhage via RAGE-NOX2/4 axis.Frontiers in neuroscience · 2024Article
- Therapeutic potential of NOX inhibitors in neuropsychiatric disorders.Psychopharmacology · 2023Review
- RAGE Inhibitors in Neurodegenerative Diseases.Biomedicines · 2023Review
- Structure, Activation, and Regulation of NOX2: At the Crossroad between the Innate Immunity and Oxidative Stress-Mediated Pathologies.Antioxidants (Basel, Switzerland) · 2023Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is the leading cause of dementia in humans, with a high social and economic cost. AD is predominantly a sporadic disease, and the intracerebroventricular (ICV) administration of streptozotocin (STZ) has been widely used as an AD-like model of dementia. While the etiology of AD remains unknown, changes such as glucose metabolism and activation of receptors for advanced glycation end products (RAGE) seem to underlie its pathogenesis. We hypothesized that methylglyoxal, an endogenous toxin derived from the glycolytic pathway, could be the precursor of advanced glycated end products that activates RAGE and that, consequently, may activate membrane NADPH oxidase (NOX), contributing to the inflammatory status of the model and the disease. We administered ICV-STZ to Wistar rats and evaluated several neurochemical parameters in the hippocampus, particularly glyoxalase 1 (GLO-1) activity, which serves as an index of high levels of methylglyoxal, and the contents of RAGE and NOX-2, the most abundant brain NOX isoform. At the times evaluated (4 and 24 weeks after STZ), we observed cognitive deficit, increased beta-amyloid content, and increased tau phosphorylation. A persistent increase in GLO-1 activity was found, as well as increases in RAGE and NOX-2 contents, suggesting astroglial and microglial commitment. The increase in NOX-2 may reflect elevated microglial activity (confirmed by IBA-1 marker), which may contribute to the synaptic dysfunction and pruning described in the literature, both in this model and AD patients. Furthermore, reinforcing this possibility, we found a reduction in cholinergic communication in the hippocampus (as shown by decreased choline acetyltransferase), a reduction in BDNF, and an increase in TGF-β, the combination of which may result in synaptic deterioration.
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