Conclusion
Treadmill exercise reduces Aβ-deposition in the skeletal muscle and improves the regulation of energy metabolism. Thus, collectively, these results suggest that exercise could be a positive therapeutic strategy for skeletal muscle dysfunction in AD patients.
Methods
At 13 months of age, NSE/PS2m mice (Tg) and control mice (non-Tg) were assigned to non-exercise control (Con) and exercise groups (Exe). The four groups were as follows: non-Tg Con, non-Tg Exe, Tg Con, and Tg Exe. The treadmill exercise was carried out for 12 weeks.
Purpose
Alzheimer's disease (AD) is classified as a progressive neurological disorder, which not only causes cognitive impairment but also abnormal weight loss, with a reduction of muscle mass related to the accumulation of amyloid-β (Aβ) in skeletal muscle. Thus, we investigated the effect of treadmill exercise on Aβ deposition, and p-AMPK, p-ACC, BDNF, and GLUT4 protein levels the regulation of muscle energy metabolism using an AD mouse.
Results
The highest levels of Aβ expression in the skeletal muscle were in the Tg Con group. Aβ expression was significantly reduced in the Tg Exe group, compared to the Tg Con group. Congo red staining showed remarkable diffuse red amyloid deposition in the Tg Con group, while Aβ-deposition in the skeletal was reduced with muscle exercise in the Tg Exe group. Exercise also increased AMPK and ACC phosphorylation and BDNF and GLUT4 expression in the skeletal muscle of non-Tg and Tg mice.