Mitochondria are a primary energy source throughout the body and therefore a decline in their function disrupts normal cellular activity and could ultimately lead to cell death. In support, we observed that aged mice showed reduced expression of mitochondrial ribosomal protein 63 , which is known to aid in protein synthesis within mitochondria. Further, we observed that exercise increased expression of MRP63. This finding is in agreement with prior work that indicates some of the beneficial effects of exercise are mediated through its influence on mitochondria. In agreement with prior reports, wheel running significantly increased expression of brain derived neurotrophic factor in both adult and aged mice. BDNF is believed to mediate the beneficial effects of exercise on cell growth, proliferation, and possibly cognitive enhancements. In addition to BDNF, we observed that a GO term related to growth was significantly enriched from exercise. For example, wheel running was found to increase expression of poly polymerase 1 and RuvB-like protein 1 , genes involved in repairing damage to DNA and maintaining genomic stability. Exercise was found to suppress expression of BCL2 binding component 3 , a gene that can initiate apoptosis. These findings confirm that exercise independent of age supports brain health by initiating growth and protection against destructive events. Collectively, these data highlight transcriptional changes that may mediate the anti-aging effects of exercise. Our findings confirm prior microarray experiments that assessed gene transcription changes in response to exercise , aging , or exercise only in aged mice. Ultimately, our findings indicate that the beneficial effects of exercise likely result from changes in multiple Ruxolitinib pathways that may be restorative in aged subjects, but also act as a preventive measure in younger subjects. The data emphasize that effective anti-aging treatments need to combat a complex array of changes. Wheel running was found to regulate chromatin structure, cell growth, immune activity, and trophic factors opposing many of the age-related changes in these categories. Findings argue that the therapeutic effects of exercise likely results from its ability to modulate a broad range of processes that are altered by normal aging. Chronic lymphocytic leukemia is characterized by the accumulation of CD5+ B lymphocytes in the blood, bone marrow and secondary lymphoid tissues. According to the current view, CLL cells are highly dependent on microenvironmental MDV3100 interactions that provide proliferative and prosurvival stimuli to the malignant cells.