Neuroinflammation induced by amyloid β25–35 modifies mucin-type O-glycosylation in the rat's hippocampus

Amyloid- β (Aβ) plays a relevant role in the neurodegenerative process of Alzheimer's disease (AD). The 25–35 peptide of amyloid-β (Aβ25–35) induces the inflammatory response in brain experimental models. Mucin-type O-glycosylation has been associated with inflammation of brain tissues in AD, thus in this work, we aimed at identifying changes in the glycosylation profile generated by the injection of Aβ25–35 into the CA1 of the hippocampus of rats, using histochemistry with lectins. Our results indicate that 100μM Aβ25–35 induce increased recognition of the Amaranthus leucocarpus lectin (ALL) (specific for Galβ1,3-GalNAcα1,0-Ser/Thr); whereas concanavalin A (Con A) (specific for α-Man) showed no differences among treated and control groups of rats.
Source: Neuropeptides - Category: Neuroscience Authors: Source Type: research