ArticleInternational journal of molecular sciences2025
Decreasing β-Catenin Leads to Altered Endothelial Morphology, Increased Barrier Permeability and Cognitive Impairment During Chronic Methamphetamine Exposure.
Article in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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
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Who cites it
1 citing paper in PubMed.
- The missing link: TNF-α as a unifying mechanism in methamphetamine-induced neuronal dysfunction and blood-brain barrier compromise.Journal of neuroimmunology · 2025Review
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Authors and funding
5 authors.
Funding
Abstract
Cognitive impairment induced by chronic methamphetamine (METH) exposure exhibits similarities to neurodegenerative disorders and is associated with blood-brain barrier (BBB) dysfunction. However, the potential involvement of β-catenin in maintaining BBB integrity during METH exposure remains unexplored. In this study, Y-maze and novel object recognition tests were conducted to assess cognitive impairment in mice exposed chronically to methamphetamine for 2 and 4 weeks. Gd-DTPA and Evans blue leakage tests revealed disruption of the BBB in the hippocampus, while chronic METH exposure for 2 and 4 weeks significantly decreased β-catenin levels along with its transcriptionally regulated protein, claudin5. Additionally, various neural injury-related proteins, such as APP, Aβ1-42, p-tau (Thr181) and p-tau (Ser396), as well as neuroinflammation-related proteins, such as IL-6, IL-1β, and TNF-α, exhibited increased levels following chronic METH exposure. Furthermore, plasma analysis indicated elevated levels of p-Tau (total), neurofilament light chain, and GFAP. In vitro experiments demonstrated that exposure to METH resulted in dose-dependent and time-dependent reductions in cellular activity and connectivity of bEnd.3 and hcmec/D3 cells. Furthermore, β-catenin exhibited decreased levels and altered subcellular localization, transitioning from the cell membrane to the cytoplasm and nucleus upon METH exposure. Overexpression of β-catenin was found to alleviate endothelial toxicity and attenuate junctional weakening induced by METH. The aforementioned findings underscore the crucial involvement of β-catenin in endothelial cells during chronic METH exposure-induced disruption of the BBB, thereby presenting a potential novel target for addressing METH-associated cerebrovascular dysfunction and cognitive impairment.
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Registered trials
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