ArticleCell reports2025
Deficiency in N-cadherin-Akt3 signaling impairs the blood-brain barrier.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Article
- Improved Sensitivity in Large Field of View Multispectral Laser-Scanning Photoacoustic Microscopy for Measuring Oxygen Saturation In Vivo.Journal of biophotonics · 2026Article
- Comparative pharmacokinetics of total ginsenosides between young and aging mice.Frontiers in pharmacology · 2026Article
- Exploring the molecular mechanism of dexmedetomidine in alleviating blood-brain barrier disruption in rats with cerebral ischemia reperfusion injury based on network pharmacology.Frontiers in molecular neuroscience · 2026Article
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Authors and funding
12 authors.
Funding
Abstract
The blood-brain barrier (BBB) restricts the passage of protein-rich fluids through tight junctions (TJs) formed between brain endothelial cells (BECs). BBB restrictiveness diminishes with aging, but the underlying mechanisms remain unclear. BECs establish physical contact with pericytes via N-cadherin homophilic adhesion. In cortex tissue from young and middle-aged patients, the age-related loss of vascular N-cadherin corresponds with the disruption of occludin TJs. Genetic deletion of N-cadherin in ECs impairs occludin TJs, leading to reduced cerebral tissue perfusion and spatial memory deficit. Mechanistically, the assembly of N-cadherin contacts stabilizes occludin TJs via the phosphoinositide 3-kinase p110β-Akt3 circuit, which is disrupted with aging. Furthermore, mutation of occludin Ser471 to Ala destabilizes occludin TJs even in the presence of N-cadherin contacts. These findings highlight a functional role for N-cadherin as a signaling hub that stabilizes occludin at TJs in a phosphorylation-dependent manner, thereby supporting BBB integrity.
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