Galectin-1 improves cognition in an animal model of Alzheimer?s disease and prevents blood-brain barrier disruption caused by exposure to Amyloid-β in vitro

JESSICA PRESA; CARLOS POMILIO; AMAL GREGOSA; ÁNGELES VINUESA; KWANG SIK KIM; JUAN BEAUQUIS; GABRIEL RABINOVICH; FLAVIA SARAVIA

Mar del Plata

Congreso; Reunión anual de la Sociedad Argentina de Investigaciones Clínicas; 2018

Alzheimer?s disease (AD) is a neurodegenerative disorder associat¬ed with an imbalance of production and clearance of amyloid-β pep¬tides (Aβ), generating amyloid plaques in the brain. Neurofibrillary tangles and inflammation in cortex and hippocampus are recognized hallmarks of the disease, in addition to microvascular alterations and dysfunction of the blood-brain barrier (BBB). The glycan-binding protein galectin-1 (Gal1) was demonstrated to have neuroprotective effects in other neurodegenerative diseases, associated with inflam¬matory modulation. It can act on immune and endothelial cells in peripheral and central nervous system. We have shown that Gal1 treatment improved cognition in PDAPPJ20, mouse model of AD , assessed by novel location recognition test (p