Role of Galectin 1 on experimental Alzheimer´s disease. Effect of treatment on amyloid deposition, neurovascular unit and cognitive performance

CARLOS JAVIER POMILIO; CARLOS DAVID CLAUSER; GABRIEL RABINOVICH; FLAVIA SARAVIA

Mar del Plata

Congreso; Reunión anual de la Sociedad Argentina de Investigación Clínica; 2016

Alzheimer´s disease (AD) is the leading cause of dementiain the elderly. Amyloid deposits and neurofibrillary tangles areamong the principal hallmarks in the cortex and the hippocampus,brain target areas of this devastating disease that lacks effectivetreatment. Neuroinflammation early compromise the componentsof the neurovascular unit in AD. Galectin-1 (Gal 1) is a glycanbinding protein which is proposed to have several properties onimmune and endothelial cells in the periphery and also in the central nervous system. Firstly, we found that astrocytes surroundingamyloid plaques were Gal1+ in the hippocampus of PDAPPJ20mouse, transgenic (Tg) model of AD. Then, we administered Gal1(i.p.9 injections of 100ug/dose) or vehicle during 3 weeks to 12month old Tg mice, when they exhibited evident plaque deposition.Age-matched non transgenic mice were used as controls. Gal1treated group improved the performance in the Novel Object Location Recognition cognitive test compared with the vehicle group.The plaque load, assessed as Congo Red + area on hippocampalslices, diminished in a significant manner in Gal1 treated mice,reaching almost 70% decrease (p