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Fig. 7 | Acta Neuropathologica Communications

Fig. 7

From: Alzheimer’s associated amyloid and tau deposition co-localizes with a homeostatic myelin repair pathway in two mouse models of post-stroke mixed dementia

Fig. 7

Stroke exacerbates amyloid plaque burden and soluble Aβ42 levels in aged stroke hAPP-SL mice. a Representative 4× stitched images of Thioflavin S (ThioS)-stained coronal brain sections of 18 mo sham- or stroke-operated hAPP-SL mice. b Quantification revealed that relative to sham-operated hAPP-SL mice, the area occupied by ThioS-labeled amyloid plaques was significantly greater in the cortex (top graph), hippocampus (middle graph), and thalamus (bottom graph) of the stroked hAPP-SL mice; no significant difference in the amount of amyloid plaques was found between the ipsilateral versus contralateral hemisphere. c Representative 10× images of Aβ42-immunolabeled deposits (arrows) in the primary somatosensory cortex of the 18 mo sham- or stroke-operated hAPP-SL mice (Equivalent = area imaged in wt-sham mice that is equivalent to the ipsilateral hemisphere imaged in wt-stroke mice). Scale bar, 125 μm. d Quantification revealed that relative to sham-operated hAPP-SL mice, the area occupied by Aβ42+ deposits was significantly higher in the cortex (top graph), thalamus (bottom middle graph), and internal capsule (bottom graph) of the stroked hAPP-SL mice (p value for the hippocampus shown in the top middle graph was 0.0751); no significant difference in the amount of Aβ42+ deposits was found between the ipsilateral versus contralateral hemisphere. e A single-plex immunoassay of tissue samples from the ipsilateral cortex or thalamus/internal capsule regions showed that in hAPP-SL mice, significantly higher levels of soluble Aβ42 are found in stroked mice compared to sham-operated mice. Data represent mean ± SEM. *p<0.05 and **p<0.01

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