Fig. 4: E4orf1 expression mediated improvement in glycemic control prevents cognition decline in older APP/PS1 mice and ameliorates brain and serum amyloid beta levels. | Nutrition & Diabetes

Fig. 4: E4orf1 expression mediated improvement in glycemic control prevents cognition decline in older APP/PS1 mice and ameliorates brain and serum amyloid beta levels.

From: E4orf1 improves adipose tissue-specific metabolic risk factors and indicators of cognition function in a mouse model of Alzheimer’s disease

Fig. 4

To determine spatial learning and memory in the 17–23-month-old APP/PS1, morris water maze test was performed. Over the 4 trials done on different days, E4orf1 expressing APP/PS1 mice show faster escape latency by finding the platform, which is significantly improved on trial day 4 compared with control APP/PS1 mice (A). There was no significant difference in time spent in the quadrant when the platform was removed (B). In 18–24-month-old E4orf1 expressing APP/PS1 mice, there was no difference in Aβ expression levels in the brain hippocampal (C, F) and frontal cortex (D, G) regions. E4orf1 expressing mice show significant reduction in serum Aβ40 levels (H) but not Aβ42 (E). These mice also show significantly reduced expression of advanced glycation end-products (AGEs)-receptor (RAGE) (L) and increased expression of amyloid beta degrading enzyme neprilysin (NEP) (J) in the cortex, but not in hippocampus (I, K), suggesting reduced Aβ production and degradation. Welch’s t test: *p < 0.05.

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