Abstract
[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. [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. [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. [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.
Highlights
The loss of brain cells in Alzheimer’s disease (AD), which is classified as a progressive neurological disorder, causes irreversible deterioration of cognitive function and loss of memory
We investigated whether treadmill exercise might reduce the accumulation of Aβ-42 protein levels and improve several molecular factors, namely, p-AMPK, p-ACC, GLUT4, and Brain-derived neurotropic factor (BDNF), which are related to energy metabolism in skeletal muscle
The expression of Aβ-42 in skeletal muscle significantly decreased in Tg mice that were subjected to treadmill exercise, compared to sedentary Tg mice (F(3,16)=106.10, p < 0.001; Fig. 2A)
Summary
The loss of brain cells in Alzheimer’s disease (AD), which is classified as a progressive neurological disorder, causes irreversible deterioration of cognitive function and loss of memory. Many previous studies have reported that the accumulation of abnormal Aβ, which is cleaved by β-and γ-secretases derived from the amyloid precursor protein (APP), provokes an outstanding increase of the neurotoxic Aβ in the brain, leading to cognitive impairments[2,3]. Accumulated Aβ in skeletal muscle contributes to motor dysfunction through muscle weakness and atrophy, which has been observed in AD as well as other disorders with associated gait disturbances[9,10]. According to these studies, the adverse effects of Aβ deposition may manifest in the brain, and in skeletal muscle
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