Fig. 8. The proposed mechanisms by which exercise delays the progression of AD.

Exercise promotes lysosomal biosynthesis by promoting nuclear translocation of TFEB, and activates the maturation of lysosomal enzymes via proteins related to vesicle trafficking, thereby improving the degradation of Aβ, maintaining the protein homeostasis, and delaying the progress of AD. Lysosomes may be a new target for non-pharmacological treatment for AD.