Fig. 9: High oxygen treatment protects from OSA-exacerbated AD phenotypes. | Nature Communications

Fig. 9: High oxygen treatment protects from OSA-exacerbated AD phenotypes.

From: Cholinergic basal forebrain degeneration due to sleep-disordered breathing exacerbates pathology in a mouse model of Alzheimer’s disease

Fig. 9

Number of cLDT (A) and cBF (B) neurons in APP/PS1 mice injected with UII-SAP and either the untreated (normoxia, normal oxygen) or treated daily with high oxygen. Number (C; P = 0.0320) and area (D; P = 0.0432) of thioflavin-S-positive Aβ plaques in the neocortex of APP/PS1 mice injected with UII-SAP and treated with normoxia or high oxygen. Density (E; P = 0.0056) and area (F; P = 0.0432) of GFAP-positive microglia in the neocortex of APP/PS1 mice injected with UII-SAP and treated with normoxia or high oxygen. Density (G; P = 0.0098) and area (H; P = 0.0264) of CD68-positive astrocytes in the neocortex of APP/PS1 mice injected with UII-SAP and treated with normoxia or high oxygen. * P < 0.05, **P < 0.01, n.s., non-significant. Student’s unpaired two-tailed t-test for panels (A–H). Results are presented as mean ± s.e.m. Each data point represents an individual animal. Source data are provided in the Source Data file.

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