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

POMILIO C; BENTIVEGNA M; RABINOVICH G; VINUESA A; MORALES R; BEAUQUIS J; CLAUSER D; SARAVIA F

Mar del Plata

Congreso; Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2016

Sociedad Argentina de Investigación Clínica (SAIC)

Alzheimer´s disease (AD) is the leading cause of dementia in the elderly. Amyloid deposits and neurofibrillary tangles are among the principal hallmarks in the cortex and the hippocampus, brain target areas of this devastating disease that lacks effective treatment. Neuroinflammation early compromise the components of the neurovascular unit in AD.Galectin-1 (Gal 1) is a glycan binding protein which isproposed to haveseveral properties on immune and endothelial cells in the periphery and also in the central nervous system. Firstly, we found that astrocytes surrounding amyloid plaques were Gal1+ in the hippocampus of PDAPPJ20 mouse, transgenic (Tg) model of AD. Then, we administered Gal1 (i.p.9 injections of 100ug/dose) or vehicle during 3 weeks to 12 month oldTg mice,when they exhibited evident plaque deposition.Age-matched nontransgenic mice were used as controls. Gal1 treated group improved the performance in the Novel Object Location Recognitioncognitivetestcompared with the vehicle group. The plaque load, assessed as Congo Red + area on hippocampal slices, diminished in a significant manner in Gal1 treated mice, reaching almost 70% decrease (p