reduced the total number of seizures experienced by the treated patients. Physical exercise increases BDNF levels via increased H3 acetylation and decreased expression of some relevant histone deacetylases. Some evidence has shown that physical exercise also has an impact on the expression of microRNAs related to neurodegeneration. The effects of microRNAs are thoroughly discussed above in the effects on cognition section. However, the mechanisms behind exercise and microRNA expression are not clear. Further study is required to understand how significant the interaction is between exercise and microRNA expression. One of the key functions of BDNF is to inhibit reactive oxygen species(ROS) which have been seen to damage cells and consequently discourage proper brain functioning. Physical exercise patients undergoing a high-intensity workout showed a notable increase in ROS that could significantly counter the benefits of moderate BDNF levels discussed prior. This finding suggests that low to moderate intensities are preferred treatment methods for those already at risk for neurological dysregulation. However, the detrimental effects of high intensity of workouts significantly diminish over time as the person naturally adapts to the oxidative stress that promotes ROS. As mentioned previously, neurogenesis impairment is both an indicator and result of neurodegenerative diseases including epilepsy. Studies have shown that subjects manipulated to experience chronic epilepsy showed a significant reduction of granule cells in the dentate gyrus, a subsection of the hippocampus critical to neurogenesis. Those same studies then demonstrated how subjects treated with physical exercise showed a return to normal-like granule cell count consequently improving neurogenesis and brain functioning. Physical exercise has demonstrated to have positive effects on the epigenetic modulation of BDNF levels and neurogenesis maintenance specifically in epileptic patients. Alzheimer's Disease Alzheimer's disease(AD) is characterized by significant decline in cognition and memory with evidence showing that physical exercise can slow its progression and even provide return of loss function(s) in some cases. One of the primary modes of AD is the loss or atypical functionality of microglia and astrocytes caused by excessive build-up of amyloid beta peptide plaque upon the brain. The amyloid beta plaque causes the microglia and astrocytes regulatory components to be improperly activated resulting in excessive and inaccurate immune response that targets healthy neurons. This interaction acts as a negative feedback loop that creates an environment prone to gross accumulation of amyloid beta plaque. Excessive amounts of amyloid beta plaque triggers improper regulatory mechanisms leading to further neuronal loss and