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Basic Science and Pathogenesis.

Jessica L Presa1,2, Carlos Javier Pomilio1,3, Eugenia Matzkin2

  • 1University of Buenos Aires, Buenos Aires, Argentina.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 24, 2025
PubMed
Summary
This summary is machine-generated.

Galectin-1 (Gal1) shows promise in treating Alzheimer's disease (AD) by protecting the blood-brain barrier and reducing amyloid buildup. This study demonstrates Gal1's potential to counteract key AD pathologies.

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Area of Science:

  • Neuroscience
  • Immunology
  • Vascular Biology

Background:

  • Alzheimer's disease (AD) involves neuroinflammation, vascular dysfunction, and impaired proteostasis.
  • Galectin-1 (Gal1), a protein with immunomodulatory and vascular roles, is a potential therapeutic agent for AD.

Purpose of the Study:

  • To evaluate Galectin-1's role in Alzheimer's disease (AD) pathophysiology.
  • To assess Gal1's therapeutic potential in both in vitro and in vivo AD models.

Main Methods:

  • Utilized human brain microvascular endothelial cells (HBMECs) and PDAPPJ20 transgenic mice.
  • Employed immunofluorescence, confocal microscopy, flow cytometry, transwell assays, RT-PCR, BBB permeability assays, and RNAseq.
  • Analyzed data using custom FIJI macros and statistical software (R/Graphpad).

Main Results:

  • Gal1 protected HBMECs from Aβ-induced blood-brain barrier (BBB) disruption and restored Aβ uptake.
  • Gal1 counteracted Aβ-induced activation of unfolded protein response and NLRP3 inflammasome pathways.
  • In vivo, Gal1 treatment reduced amyloid deposition, improved BBB integrity, and restored transcriptional profiles in AD mice.

Conclusions:

  • Galectin-1 acts as a pleiotropic modulator of AD pathology, particularly affecting microvascular changes.
  • Gal1-based strategies may offer a multi-level therapeutic approach for the complex pathology of AD.