RECOVERY OF ASTROCYTE-VASCULAR COMMUNICATION IN THE HIPPOCAMPUS OF MICE WITH CEREBRAL AMYLOID ANGIOPATHY FOLLOWING TREATMENT WITH THE GLYCAN-BINDING PROTEIN GALECTIN-1

PRESA, JESSICA; POMILIO, CARLOS; CAMILA OSES; GREGOSA, AMAL; BENTIVEGNA, MELISA; BELLOTTO, MELINA; PÉREZ, NICOLÁS GONZÁLEZ; VINUESA, ANGELES; BEAUQUIS, J; VALERIA LEVI; MARIANO SOIZA-REILLY; RABINOVICH G; FLAVIA EUGENIA SARAVIA

Mar del Plata

Congreso; Reunion Anual de la Sociedad Argentina de Investigacion Clinica; 2023

SAIC

Cerebral amyloid angiopathy (CAA) is caused by amyloid perivascular deposition. In Alzheimer’s Disease (AD), CAA is found inarteries, arterioles and capillaries, being detrimental to their function and correlating with disease progression. Clinical interventionswould benefit from restoring vascular changes. Galectins, a familyof `-galactoside-binding proteins, play key roles in regulating immune, neuronal and vascular circuits. The neuroprotective effectsof Galectin-1 (Gal1) in a model of CNS autoimmune inflammation,led us to explore its potential role in AD. Tg PDAPPJ20 mice-CAA/AD model- were treated with recombinant Gal1 (rGal1; three weekly i.p. 9 injections; 100 ug). Vehicle-treated 12 months-old Tg-miceshowed large amyloid deposition around vessels on the hilus of thehippocampus, a highly vascularized region affected early duringAD. Notably, Tg mice treated with rGal1 (Tg-Gal1) exhibited a 35%decrease in amyloid deposition around vessels compared to TgVeh (p