ArticleCurrent research in toxicology2025
RhoA/ROCK2 signaling pathway regulates Mn-induced alterations in tight junction proteins leading to cognitive dysfunction in mice.
Article in Current research in toxicology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- RhoA/ROCK signaling as a potential convergent pathway in microbiota-gut-brain axis-related cognitive impairment.Frontiers in neurology · 2026Review
- Evaluation of 5-hydroxytryptamine (5-HT) on Cognitive Function in Rats with Gut-Brain Axis Dysfunction Following Acceleration Exposure.Molecular neurobiology · 2025Article
- Article
- Manganese-Induced Parkinsonism: A Review of Etiologies and Treatments.Degenerative neurological and neuromuscular disease · 2025Review
- Gut to brain: essential micronutrient and trace element manganese transport, function and toxicity.Frontiers in physiology · 2025Review
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Authors and funding
7 authors.
Funding
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Abstract
Elevated manganese (Mn) exposure has been implicated in a broad spectrum of neurological disorders, including motor dysfunction and cognitive deficits. Previous studies have demonstrated that Mn induces neurotoxicity by disrupting the integrity of the blood-brain barrier (BBB), a critical regulator in maintaining central nervous system homeostasis and a contributing factor in the pathogenesis of numerous neurological disorders. However, the precise molecular mechanisms underlying Mn-induced BBB disruption and its role in facilitating neurotoxicity remain incompletely understood. The primary objectives of this study were to elucidate the mechanisms underlying the relationship between Mn exposure and BBB tight junction proteins (TJPs), and to further investigate potential neuroprotective strategies for mitigating Mn-induced cognitive impairments. In this investigation, we developed Mn exposure models utilizing both murine subjects and cell culture systems to elucidate the mechanisms underlying TJPs involvement and to assess the potential neuroprotective effects of gastrodin (GAS), a bioactive compound extracted from traditional Chinese medicine. Our findings revealed a significant reduction in TJPs expression, both
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