Treadmill exercise induces age-related changes in aversive memory, neuroinflammatory and epigenetic processes in the rat hippocampus

Running-induced Functional Mobility Improvement in the Elderly Males is Driven by Enhanced Plasma BDNF Levels and the Modulation of Global Histone H4 Acetylation Status

“…On the other hand, a recent study (30) reported no difference in histone H4 acetylation levels between middle-aged runners and sedentary individuals. These findings were in agreement with the experimental studies reporting that histone acetylation status in response to exercise might act in an age-dependent manner (8,36).…”

“…Likewise, a significant increase on global histone H4 acetylation levels was observed in the hippocampus of aged rats submitted to a chronic protocol running on a treadmill (8). Emerging clinical evidence also showed that exercise is an epigenetic modulator in a lot of tissue, including peripheral blood (19,24).…”

“…Histone acetyltransferases (HATs) and histone deacetylates (HDACs), respectively, add and remove the acetyl groups of lysine residues from amino-terminal tails of histones (7). In this context, Lovatel et al demonstrated that lower levels of global histone H4 acetylation were found in hippocampi from aged rats (8), suggesting that this epigenetic mark might be associated with the aging process. growth and development, and is involved with learning/memory processes and motor improvement (9)(10)(11).…”

Exercise as a pro-cognitive, pro-neurogenic and anti-inflammatory intervention in transgenic mouse models of Alzheimer’s disease

“…Aged male Wistar rats were impaired in the inhibitory avoidance task compared to their adult counterparts. The authors of the study identified a correlation between expression of pro-inflammatory cytokines and cognitive performance, with increased hippocampal IL-1␤ and TNF-␣ detected in aged rat samples (Lovatel et al, 2013). Specifically focusing on IL-1␤, impairments in long-term contextual and spatial memory were observed in a transgenic model of IL-1␤ overexpression.…”

Therapeutics with SPION-labeled stem cells for the main diseases related to brain aging: a systematic review

“…81 Genetics, in addition to lifestyle also play central roles in this process. 82 There are several studies suggesting an increased expression in miRNA network that modulates the inflammatory profile of neural and glial cells, also affecting behavioral aspects and, therefore, influences the epigenetics, 79,83 or the cells' telomerase activity by accelerating or slowing down the process of cerebral aging. 84 In this sense, accelerated brain aging by environmental components, behavioral or genetic, makes the brain structure vulnerable to two distinct disease processes, which are associated in some situations: i) oxidative stress modulating the chronic accumulation of protein clusters (a-synuclein, β amyloid, Tau, etc) or intracellular apoptotic/degenerative events by the increased immune response, and ii) the ischemic event, acute in most situations, caused by trauma or thromboembolic events.…”