Neuroinflammation induced by the peptide amyloid-β (25-35) increase the presence of galectin-3 in astrocytes and microglia and impairs spatial memory.

Galectins are animal lectins that bind to β-galactosides, such as lactose and N-acetyllactosamine, contained in glycoproteins or glycolipids. Galectin-1 (Gal-1) and Galectin-3 (Gal-3) are involved in pathologies associated with the inflammatory process, cell proliferation, adhesion, migration, and apoptosis. Recent evidence has shown that the administration of Amyloid-β 25-35 (Aβ25-35) into the hippocampus of rats increases the inflammatory response that is associated with memory impairment and neurodegeneration. Galectins could participate in the modulation of the neuroinflammation induced by the Aβ25-35. The aim of this study was to evaluate the presence of Gal-1 and Gal-3 in the neuroinflammation induced by administration of Aβ25-35 into the hippocampus and to examine spatial memory in the Morris water maze. After the administration of Aβ25-35, animals were tested for learning and spatial memory in the Morris water maze. Behavioral performance showed that Aβ25-35 didn't affect spatial learning but did impair memory, with animals taking longer to find the platform. On the day 32, hippocampus was examined for astrocytes (GFAP), microglia (Iba1), Gal-1 and Gal-3 via immunohistochemical analysis, and the cytokines IL-1β, TNF-α, IFN-γ by ELISA. This study's results showed a significant increase in the expression of Gal-3 in the microglia and astrocytes, while Gal-1 didn't increase in the dorsal hippocampus. The expression of galectins is associated with increased cytokines in the hippocampal formation of Aβ25-35 treated rats. These findings suggest that Gal-3 could participate in the inflammation induced by administration of Aβ25-35 and could be involved in the neurodegeneration progress and memory impairment.