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Fig. 2 | Translational Neurodegeneration

Fig. 2

From: Recent advances on the molecular mechanisms of exercise-induced improvements of cognitive dysfunction

Fig. 2

Exercise benefits the stability of neuronal mitochondria and improves the oxidative stress and energy supply. ① Mitochondrial biogenesis: exercise can promote the AMPK/SIRT1/ PGC-1α pathway, recruit more NRF1/2 and then upregulate the mitochondrial gene expression. ② Fusion and fission: exercise can improve the fusion and fission proteins in mitochondria, such as Opa1/2, Mfn1/2, Mff, and Fis1. These proteins are especially important for the “metabolism” of mitochondria. ③ Mitophagy: exercise can promote the PINK/parkin pathway of mitophagy in the outer mitochondrial membrane (OMM). ④ After exercise, more NADH is converted to NADH+, resulting in the acetylation of FOXO1. This urges PINK1 to recruit more Parkin in the OMM to remove damaged mitochondria

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Translational Neurodegeneration

ISSN: 2047-9158

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