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Figure 3 | Molecular Brain

Figure 3

From: Metabotropic glutamate receptor 5 knockout reduces cognitive impairment and pathogenesis in a mouse model of Alzheimer's disease

Figure 3

Aβ formation and plaque number is reduced in 12 month old APPswe/PS1ΔE9 mice following the genetic deletion of mGluR5. Shown in (A) is the concentration of whole brain β amyloid oligomer (ng/mg protein) concentrations in 12 month old wild-type (wt) and APPswe/PS1ΔE9 (APPswe) mice on either mGluR5+/+or mGluR5-/- genetic backgrounds. Data represents the mean ± SEM of four independent experiments. The * indicates statistically significant (p < 0.05) differences between β amyloid oligomer concentrations in APPswe/PS1ΔE9 mouse brains as compared with mice that do not express APPswe/PS1ΔE9. The ψ indicates statistically significant differences between β amyloid oligomer concentrations in APPswe mice that express mGluR5 as compared to APPswe mice that lack mGluR5 expression. Also shown are representative images of Aβ plaques in the cortex and hippocampus of 12 month old coronal brain slices from (B) APPsweand (C) APPswe/mGluR5-/- mice. Scale bar is 900 μm. (D) The graph shows the number of plaques counted 8100 μm2 regions of interests in the cortex and hippocampus in coronal brain slices from 12 month old APPswe and APPswe/mGluR5-/- mice. (E) Representative immunoblot and quantification of APP expression in wt and APPSwe mice either expressing or lacking mGluR5 expression. Data represents the mean ± SEM of four independent experiments. The * indicates statistically significant (p < 0.05) differences between APPswe expressing mGluR5 as are compared with APPswe lacking mGluR5 expression.

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