ArticleNeurotoxicity research2022
Acute Methylglyoxal-Induced Damage in Blood-Brain Barrier and Hippocampal Tissue.
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 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Methylglyoxal Accumulation is Associated with Brain Inflammation after Myocardial Infarction with Sex and Regional Differences.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Methylglyoxal, a Knot to Be Untied in Brain Glucose Hypometabolism.Metabolites · 2025Review
- Increased Levels of Circulating Methylglyoxal Have No Consequence for Cerebral Microvascular Integrity and Cognitive Function in Young Healthy Mice.Molecular neurobiology · 2025Article
- Methylglyoxal Formation-Metabolic Routes and Consequences.Antioxidants (Basel, Switzerland) · 2025Review
- Elucidating the Antiglycation Effect of Creatine on Methylglyoxal-Induced Carbonyl Stress In Vitro.International journal of molecular sciences · 2024Article
- Metabolic Reprogramming of Astrocytes in Pathological Conditions: Implications for Neurodegenerative Diseases.International journal of molecular sciences · 2024Review
- Changes in Astroglial Water Flow in the Pre-amyloid Phase of the STZ Model of AD Dementia.Neurochemical research · 2024Article
- How S100B crosses brain barriers and why it is considered a peripheral marker of brain injury.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Methylglyoxal, a highly reactive dicarbonyl compound, as a threat for blood brain barrier integrity.Fluids and barriers of the CNS · 2023Review
- Organophosphate pesticide-induced toxicity through DNA damage and DNA repair mechanisms.Molecular biology reports · 2023Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methylglyoxal (MG) is a reactive dicarbonyl compound formed mostly via the glycolytic pathway. Elevated blood glucose levels can cause MG accumulation in plasma and cerebrospinal fluid in patients with diabetes mellitus and Alzheimer's disease. Under these disease conditions, the high reactivity of MG leads to modification of proteins and other biomolecules, generating advanced glycation end products (AGEs), which are considered mediators in neurodegenerative diseases. We investigated the integrity of the blood-brain barrier (BBB) and astrocyte response in the hippocampus to acute insult induced by MG when it was intracerebroventricularly administered to rats. Seventy-two hours later, BBB integrity was lost, as assessed by the entry of Evans dye into the brain tissue and albumin in the cerebrospinal fluid, and a decrease in aquaporin-4 and connexin-43 in the hippocampal tissue. MG did not induce changes in the hippocampal contents of RAGE in this short interval, but decreased the expression of S100B, an astrocyte-secreted protein that binds RAGE. The expression of two important transcription factors of the antioxidant response, NF-κB and Nrf2, was unchanged. However, hemeoxigenase-1 was upregulated in the MG-treated group. These data corroborate the idea that hippocampal cells are targets of MG toxicity and that BBB dysfunction and specific glial alterations induced by this compound may contribute to the behavioral and cognitive alterations observed in these animals.
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What Socratic holds
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 Socratic graph.