Extended Data Fig. 9: Modulating hexosamine pathway activity does not alter astrocytosis or amyloid plaque burden in 5xFAD mice.
From: Hyperglycosylation is a metabolic driver of Alzheimer’s disease
a, Immunofluorescence images of GFAP and Aβ in hippocampus and cortex from 5xFAD-shScr and 5xFAD-shPGM3 mice. b, Quantification of reactive astrocytes and β-amyloid plaques in hippocampus and cortex showing no significant differences between 5xFAD-shScr (n = 3 animals) and 5xFAD-shPGM3 (n = 3 animals) groups. c, GFAP and Aβ staining in 5xFAD mice treated with water or glucosamine. d, Quantification of reactive astrocytes and β-amyloid plaques in hippocampus and cortex indicating similar levels between water- (n = 3 animals) and glucosamine-treated (n = 3 animals) 5xFAD mice. e, GFAP and Aβ staining in 5xFAD mice treated with saline or NGI-1. f, Quantification of reactive astrocytes and β-amyloid plaques in cortex and hippocampus showing no significant effect of NGI-1 (n = 5 animals per group). Data are mean ± s.e.m.; P values are indicated (two-tailed t-test).
