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Peer-reviewedCC BY 4.0Frontiers in Neurology

Endothelial glycocalyx remodeling and galectin signaling in aging associated epilepsy

  • Adam Legradi1
  • Cristiana Pareo2
  • Mohd Yaqub Mir3
  1. 1Department of Cell Biology and Molecular Medicine, University of Szeged
  2. 2Department of Neuroscience and Rehabilitation, University of Ferrara
  3. 3Epilepsy Centre, Department of Clinical Sciences, Lund University Hospital
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Abstract

Physiological aging can alter the brain endothelial glycocalyx and blood–brain barrier (BBB), while experimental seizures independently engage galectin-3 (Gal-3) and inflammasome-associated inflammatory signaling. This narrative review critically examines whether these observations justify a shared mechanism in aging-associated epilepsy. Primary studies support endothelial mucin-type O-glycosylation as a determinant of BBB integrity and Gal-3 as a modulator of inflammation in selected seizure models. They do not establish that endothelial glycan remodeling changes Gal-3 binding or initiates epileptogenesis. We distinguish extracellular galectin-glycan recognition from intracellular inflammasome signaling and address the anatomical separation between parenchymal microglia and the luminal glycocalyx. Glycan elongation, ligand density, terminal modifications, and steric accessibility could alter binding in different directions; uniform exposure of galectin ligands cannot be assumed. Galectin-1 also has context-dependent protective and detrimental effects. We propose compartment-resolved experiments combining glycan measurements, cell-specific perturbations, BBB assessment, and longitudinal electroencephalography to test the convergence hypothesis.

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Cite

BibTeXRIS
BibTeX
@article{legradi2026endothelial,
  title = {{Endothelial glycocalyx remodeling and galectin signaling in aging associated epilepsy}},
  author = {Adam Legradi and Cristiana Pareo and Mohd Yaqub Mir},
  journal = {Frontiers in Neurology},
  year = {2026},
  month = oct,
  doi = {10.3389/fneur.2026.1961370},
  url = {https://www.frontiersin.org/articles/10.3389/fneur.2026.1961370/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Endothelial glycocalyx remodeling and galectin signaling in aging associated epilepsy
AU  - Adam Legradi
AU  - Cristiana Pareo
AU  - Mohd Yaqub Mir
PY  - 2026
DA  - 2026/10/19
JO  - Frontiers in Neurology
DO  - 10.3389/fneur.2026.1961370
UR  - https://www.frontiersin.org/articles/10.3389/fneur.2026.1961370/full
AB  - Physiological aging can alter the brain endothelial glycocalyx and blood–brain barrier (BBB), while experimental seizures independently engage galectin-3 (Gal-3) and inflammasome-associated inflammatory signaling. This narrative review critically examines whether these observations justify a shared mechanism in aging-associated epilepsy. Primary studies support endothelial mucin-type O-glycosylation as a determinant of BBB integrity and Gal-3 as a modulator of inflammation in selected seizure models. They do not establish that endothelial glycan remodeling changes Gal-3 binding or initiates epileptogenesis. We distinguish extracellular galectin-glycan recognition from intracellular inflammasome signaling and address the anatomical separation between parenchymal microglia and the luminal glycocalyx. Glycan elongation, ligand density, terminal modifications, and steric accessibility could alter binding in different directions; uniform exposure of galectin ligands cannot be assumed. Galectin-1 also has context-dependent protective and detrimental effects. We propose compartment-resolved experiments combining glycan measurements, cell-specific perturbations, BBB assessment, and longitudinal electroencephalography to test the convergence hypothesis.
SN  - 1664-2295
ER  -