decline in function. Studies have shown, in animal models and human patients alike, that consistent exercise inhibited the improper microglial activation mentioned previously through the production of certain myokines. Muscle cells respond to contractions by releasing molecules called myokines, one of which is critical to regulating microglial response, IL-6. This myokine is produced in response to consistent exercise and has direct influence on the up or down regulation of the inflammatory response involved in neuronal loss depending on signaling pathways. Also, IL-6 provokes the production of a cytokine known as IL-10 which can prevent the activation of microglia by blocking its receptors, effectively inhibiting harmful microglial activation mentioned prior. A number of patients afflicted by neurodegenerative diseases like AD have notably lower counts of IL-6 which could explain higher instances of dysfunctional inflammatory response. Although IL-6 can be artificially induced, long-term exercise is a non-pharmaceutical approach capable of producing IL-6 levels sufficient for normal regulatory processes. Similar to epilepsy, exercise has increased BDNF levels in AD patients that were previously lacking. Physical exercise increases BDNF levels by increasing H3 acetylation and decreasing some relevant histone deacetylases. Brain-derived neurotrophic factor significantly reduces the neuroinflammation strongly associated with Alzheimer's disease and other disorders. Physical exercise can play a critical role in regulating inflammatory pathways through the epigenetic modulation of myokine IL-6 and BDNF in AD patients. Effects on psychotic disorders Schizophrenia Schizophrenia is characterized by hallucinations, delusions, paranoia, and mood disorder symptoms with evidence showing that physical exercise can alleviate neuroinflammation that could be a root cause of this affective disorder. Although it is still uncertain what exactly causes this disorder, several explanations exist such as the dopaminergic and glutamatergic hypotheses. The dopaminergic hypothesis states that schizophrenia is caused by presynaptic dopamine dysregulation. This dysregulation stems from an abnormal increase in key dopamine receptors that results in its excessive release. The glutamatergic hypothesis was previously believed to be closely tied to excessive dopamine release mentioned. However, recent literature finds that the dysfunction of N-methyl-D-aspartate receptors(NMDAR) can serve as the mechanism behind schizophrenia. Dysfunction of NMDAR receptors causes increased levels of glutamate at non-NMDA sites. Higher generalized glutamate levels in the prefrontal cortex results in atypically high signaling at AMPA receptors. Abnormal signaling activity at the AMPA receptors disrupts cell excitability believed to be connected to schizophrenia. A relatively new explanation within the topic focuses on dysfunctional neuroinflammation pathways and oxidative stress similar