Early life stress (ELS) encompasses exposure to aversive experiences during early development, such as neglect or maltreatment. Animal and human studies indicate that ELS has maladaptive effects on brain development, leaving individuals more vulnerable to developing behavioral and neuropsychiatric disorders later in life. This result occurs in part to disruptions in Brain derived neurotrophic factor (Bdnf) gene regulation, which plays a vital role in early neural programming and brain health in adulthood. A potential treatment mechanism to reverse the effects of ELS on Bdnf expression is aerobic exercise due to its neuroprotective properties and positive impact on Bdnf expression. Aerobic exercise opens the door to exciting and novel potential treatment strategies because it is a behavioral intervention readily and freely available to the public. In this review, we discuss the current literature investigating the use of exercise interventions in animal models of ELS to reverse or mitigate ELS-induced changes in Bdnf expression. We also encourage future studies to investigate sensitive periods of exercise exposure, as well as sufficient duration of exposure, on epigenetic and behavioral outcomes to help lead to standardized practices in the exercise intervention field.
Early life stress (ELS) in the form of trauma or caregiver abuse and neglect is often associated with psychopathology. However, not everyone exposed to ELS develops a pathology; others display resilience, or the ability to adapt and persevere despite ongoing adversity. Several molecular moderator variables between ELS and behavioral phenotypes have been proposed, including single nucleotide polymorphisms (SNPs) and epigenetic markers. Specifically, several SNPs and aberrant methylation or expression of genes associated with neurotransmitter systems and brain-derived neurotrophic factor have been associated with anxiety, depression or schizophrenia. The present review seeks to explore the relationship between SNPs, epigenomics and disease, and offer data to suggest several SNPs may also predict specific treatment efficacy and psychological resilience. Due to this discrepancy in the literature, it is critical that environmental moderators be equally considered in determining the ontology of resilient or pathological phenotypes; this includes the infant-caregiver relationship, and the degree of control, magnitude, and type of the stressor experienced. Finally, we will offer evidence to suggest that several intervention strategies, including drug treatment, environmental enrichment, or exercise can ameliorate many of the psychological, biological, and molecular consequences of ELS exposure, and help shift one toward a resilient phenotype.
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