Recovery of astrocyte-vascular communication in the hippocampus of mice with cerebral amyloid angiopathy following treatment with the glycan-binding protein galectin-1

PRESA J; POMILIO C; OSES C; GREGOSA A; BENTIVEGNA M; BELLOTTO M; GONZALEZ PEREZ N; VINUESA A; BEAUQUIS J; LEVI V; SOIZA REILLY M; RABINOVICH G; SARAVIA F

Mar del Plata

Congreso; Reunión Anual de Sociedades de Biociencias; 2022

Sociedad Argentina de Investigación Clínica (SAIC)

Cerebral amyloid angiopathy (CAA) is caused by amyloid perivasculardeposition. In Alzheimer’s Disease (AD), CAA is found inarteries, arterioles and capillaries, being detrimental to their functionand 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 weeklyi.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 Tg-Veh (p