EE causes an anticipation of the extracellular amyloid deposition in hippocampus and entorhinal cortex of APP^Swe/PS1^L166P mice.

<p>Left panels: quantitative analysis of amyloid load in the extracellular compartment in hippocampus (A; B), entorhinal (C; D) and primary motor cortex (E; F) in terms of plaque number (A; C; E) and plaque size (B; D; E) in 2-, 4- and 6-month-old APP^Swe/PS1^L166P mice after SE or EE. The analysis showed a significantly higher number of plaques after 2 and 4 months spent in EE since birth for hippocampus (A) and entorhinal cortex (C) but not for primary motor cortex (E). No significant difference was present in terms of plaque size in hippocampus (B), entorhinal (D) or primary motor cortex (F) (n = 5 in each group, three sections per mouse, three frames per section, <i>* P</i><0.05, *** <i>P</i><0.001, Student’s <i>t</i>-test). Error bars represent SEM. Right panels: representative images of coronal hippocampal (G; H), entorhinal (I; J) and primary motor cortical (K; L) sections of 4-month-old APP^Swe/PS1^L166P mice reared in SE (G; I; K) or in EE (H; J; L), immunostained with 6E10 antibody. Note the higher number of plaques in hippocampus and in entorhinal cortex after 2 or 4 months spent in EE. The same difference is not present in primary motor cortex. Calibration bars, 300 µm. (HIP, hippocampus; EC, entorhinal cortex; PMC, primary motor cortex; SE, Standard Environment; EE, Enriched Environment).