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Fig. 10 | Acta Neuropathologica Communications

Fig. 10

From: Cognitively impaired aged Octodon degus recapitulate major neuropathological features of sporadic Alzheimer’s disease

Fig. 10

AD-like aged degu brain displays enhanced neuroinflammation relative to controls. ah Reactive astrocytes and microglia measured by GFAP and IBA1 immunoreactivity, exhibit relatively lower intensity in control non-AD (a, e) compared to AD-like (bd, fh) aged degu coronal brain sections in confocal microscopic images. Higher magnified images show either colocalization of GFAP or IBA1 with Aβ aggregates stained by mOC23 (red) or 6E10 (red) in plaques or accumulation surrounding plaques (c, g) and vasculatures (d, h) as indicated by arrows in AD-like degu brains. i Imaris-based 3D reconstructions of representative GFAP-positive astrocytes from Non-AD and AD-like aged degu brain cortex. j, k Quantification of GFAP- (j) or IBA1-positive (k) cells in somatosensory cortex (SSC) and hippocampus shows a significant increase in both GFAP and IBA1 volumes in AD-like compared to Non-AD aged degu brains. (l-n) Sholl analysis conducted using Imaris in the filament reconstruction mode shows two representative IBA1-positive microglia from Non-AD and AD-like aged degu brain cortex (i), respectively; mean distribution plots of Sholl intersection numbers versus the distance from the microglial soma demonstrate a significant decrease in the total number of intersections of microglial cells in both in cortex (somatosensory cortex) (m) and hippocampus (n) in AD-like aged degu brains compared to age-matched Non-AD degus. The scale bar represents 100 μm (a, b, e, f) and 40 μm (c, d, g, h). p < 0.01*, 0.001**, or 0.0001***

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