Physical exercise improves brain cortex and cerebellum mitochondrial bioenergetics and alters apoptotic, dynamic and auto(mito)phagy markers

The rate of training response to aerobic exercise affects brain function of rats

“…The question arises whether the increased apoptosis in LRTE rats is a protective or pathological event. Exercise reported to decrease Bax/Bcl-2 ratio (Marques-Aleixo et al, 2015), and this tendency was visible in HRTE group and this is accordance with the neuroprotective role of exercise.…”

Effect of treadmill exercise on PI3K/AKT/mTOR, autophagy, and Tau hyperphosphorylation in the cerebral cortex of NSE/htau23 transgenic mice

“…Lastly, LC3-B is known to control the completion stage of autophagosome formation; its expression was found to be reduced in the Tg-CON group compared with that in the NonTg-CON group, whereas its expression was increased in the Tg-TE group. The increase of LC3 II expression after treadmill exercise was consistent with the findings of previous studies showing that exercise might induce autophagy [46,47]. In other words, the abnormal autophagy in NSE/htau23 transgenic mice was found to be ameliorated by treadmill exercise.…”

“…Thus, directly comparing their results with those of the present study is difficult. In addition, Marques-Aleixo et al [47] reported that, compared between normal mice subjected to treadmill exercise and voluntary wheel running and the control group, there was no statistically significant difference in the expression of p62 in the cerebral cortex and hindbrain areas. Therefore, the results of this study suggest that, although autophagy is inhibited by over-expression of p62 protein in NSE/htau23 mice, the autophagy process of p62 protein was normally induced via a treadmill exercise performed for 12 weeks with progressive loading.…”

Myoinositol Attenuates the Cell Loss and Biochemical Changes Induced by Kainic Acid Status Epilepticus

“…Increase in the amount of VDAC-1 and M-cofilin could lead to the changes in mitochondrial permeability transition pore, with increased escape of cytochrome c to cytoplasm and activation of caspase cascade, including caspase-3. It is interesting to note that the same types of changes were observed in rat brain with endurance treadmill training—this exercise decreases the amounts of VDAC-1, cofilin, and caspase-3 alongside with other markers of oxidative stress and apoptotic signaling, whereas no changes were found in CO-I [41]. …”