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The natural aging process as well as many age-related diseases is associated with impaired metabolic adaptation and declined ability to cope with stress. As major causes of disability and morbidity during the aging process, brain disorders, including psychiatric and neurodegenerative disorders, are likely to increase across the globe in the future decades. This narrative review investigates the link among exercise and brain disorders, aging, and inflammatory biomarkers, along with the function of brain-derived neurotrophic factor. For this study, related manuscript from all databases, Google scholar, Scopus, PubMed, and ISI were assessed. Also, in the search process, the keywords of exercise, neurodegeneration, neurotrophin, mitochondrial dysfunction, and aging were used. Mitochondrial abnormality increases neuronal abnormality and brain disease during the aging process. Stress and inflammatory factors caused by lifestyle and aging also increase brain disorders. Evidences suggest that exercise, as a noninvasive treatment strategy, has antioxidant effects and can reduce neuronal lesions. Brain-derived neurotrophic factor expression following the exercise can reduce brain symptoms; however, careful consideration should be given to a number of factors affecting the results. [ABSTRACT FROM AUTHOR]

Epigenetics, or alterations in the phenotype or gene expression due to mechanisms other than changes in the underlying DNA sequence, reflects the sensitivity and responsiveness of human and animal brains in constantly varying circumstances regulating gene expression profiles that define the biomarkers and present the ultimate phenotypical outcomes, such as cognition and emotion. Epigenetics is associated with functionally relevant alterations to the genome in such a fashion that under the particular conditions of early, adolescent, and adult life, environmental signals may activate intracellular pathways that remodel the 'epigenome,' triggering changes in gene expression and neural function. Thus, genetic influences in neuropsychiatric disorders that are subject to clinical staging, epigenetics in schizophrenia, epigenetic considerations in the expression of sensorimotor gating resulting from disease conditions, biomarkers of drug use and addiction, current notions on the role of dopamine in schizophrenia spectrum disorders, and the discrete interactions of biomarkers in persistent memory were to greater or lesser extents reflected upon. The relative contributions of endophenotypes and epistasis for mediating epigenetic phenomena and the outcomes as observed in the analysis of biomarkers appear to offer a multitude of interactive combinations to further complicate the labyrinthine machinations of diagnosis, intervention, and prognosis. [ABSTRACT FROM AUTHOR]