Recovered astrocyte-vascular communication in the hippocampus of AD-mice after glycan-binding protein Galectin-1 treatment

PRESA, J.; POMILIO, C.; VINUESA, A.; BENTIVEGNA, M.; GONZÁLEZ PÉREZ, N.; BELLOTTO, M.; SOIZA-RELLY, M.; BEAUQUIS, J.; RABINOVICH, G.; SARAVIA, F.

Congreso; Encuentro Bianual de la International Society for Neurochemistry; 2023

Cerebral amyloid angiopathy (CAA) is caused by amyloid perivascular deposition. In Alzheimer's Disease (AD), CAA is found in arteries, arterioles and capillaries, being detrimental to their function. AD's vascular alterations correlate with disease progression. Clinical interventions would benefit from preventing or restoring vascular changes. Galectins, a family of galactosidebinding proteins, are involved in survival, immune and vascular pathways. Galectin-1 (Gal1) positive effects on an autoimmune encephalomyelitis model, lead us to explore a potential role in AD. Tg PDAPPJ20 mice, a model for CAA/AD, received a treatment of Gal1 (three weekly i.p. 9 injections of 100 ug/dosis). Tg 12 m.o mice vehicle-treated (Tg-Veh) showed considerable amyloid deposited around vessels on the hilus of the hippocampus, a highly vascularized region early susceptible in AD. However, Tg mice treated with Gal1 (Tg-Gal1) presented a 35% decrease compared to Tg-Veh (p