Galectin-1 reduces hippocampal amyloid deposits and controls the neurovascular unit in a transgenic mouse model of Alzheimer's Disease

JESSICA PRESA; CARLOS POMILIO; JUAN BEAUQUIS; ÁNGELES VINUESA; MELISA BENTIVEGNA; AMAL GREGOSA; ROSA MORALES; GABRIEL RABINOVICH; FLAVIA SARAVIA

Buenos Aires

Congreso; Congreso Anual de la Sociedad Argentina de Investigaciones Clínicas; 2017

Sociedad Argentina de Investigación en Neurociencias

Alzheimer?s disease (AD) is the most common form of dementia. Although the pathogenesis of AD remains cryptic, this pathology is associated with an imbalance in the production and clearance of amyloid-β protein (Aβ). Aβ deposition and neuroinflammation are recognized hallmarks in AD, affecting mainly the brain cortex and hippocampus, both in patients and animal models. The glycan-binding protein galectin-1 (Gal1) modulates several properties on immune and endothelial cells in peripheral and central nervous system compartments, where a neuroprotective role was proposed in experimental settings of autoimmune encephalomyelitis. Here, we administered Gal1 or vehicle control (i.p. 9 injections of 100 ug/dose) during 3 weeks to 12 months-old PDAPPJ20 transgenic mice, or age-matched non-transgenic animals. The Gal1 treated group displayed a significantly improved cognitive response in the Novel Object Location Recognition test (p