Mild traumatic brain injuries (mTBI) have been associated with long-term cognitive deficits relating to trauma-induced neurodegeneration. These long-term deficits include impaired memory and attention, changes in executive function, emotional instability and sensorimotor deficits. Furthermore, individuals with concussions show a high co-morbidity with a host of psychiatric illnesses (e.g. depression, anxiety, addiction) and dementia. The neurological damage seen in mTBI patients is the result of the direct impact and mechanical injury, followed by a delayed neuroimmune response that can last hours, days and even months after the injury. As part of the neuroimmune response, a cascade of pro- and anti-inflammatory cytokines are released and can be detected at the site of injury as well as subcortical, and often contralateral, regions. It has been suggested that the delayed neuroinflammatory response to concussions is more damaging then the initial impact itself. However, evidence exists for favourable consequences of cytokine production following traumatic brain injuries as well. In some cases, treatments that reduce the inflammatory response will also hinder the brain's intrinsic repair mechanisms. At present, there is no evidence-based pharmacological treatment for concussions in humans. The ability to treat concussions with drug therapy requires an in-depth understanding of the pathophysiological and neuroinflammatory changes that accompany concussive injuries. The use of neurotrophic factors (e.g. nerve growth factor) and anti-inflammatory agents as an adjunct for the management of post-concussion symptomology will be explored in this review.

Stress was once defined as the non-specific result of the body to any demand or challenge to homeostasis. A more current view of stress is the behavioral and physiological responses generated in the face of, or in anticipation of, a perceived threat. The stress response involves activation of the sympathetic nervous system and recruitment of the hypothalamic-pituitary-adrenal (HPA) axis. When an organism encounters a stressor (social, physical, etc.), these endogenous stress systems are stimulated in order to generate a fight-or-flight response, and manage the stressful situation. As such, an organism is forced to liberate energy resources in attempt to meet the energetic demands posed by the stressor. A change in the energy homeostatic balance is thus required to exploit an appropriate resource and deliver useable energy to the target muscles and tissues involved in the stress response. Acutely, this change in energy homeostasis and the liberation of energy is considered advantageous, as it is required for the survival of the organism. However, when an organism is subjected to a prolonged stressor, as is the case during chronic stress, a continuous irregularity in energy homeostasis is considered detrimental and may lead to the development of metabolic disturbances such as cardiovascular disease, type II diabetes mellitus and obesity. This concept has been studied extensively using animal models, and the neurobiological underpinnings of stress induced metabolic disorders are beginning to surface. However, different animal models of stress continue to produce divergent metabolic phenotypes wherein some animals become anorexic and lose body mass while others increase food intake and body mass and become vulnerable to the development of metabolic disturbances. It remains unclear exactly what factors associated with stress models can be used to predict the metabolic outcome of the organism. This review will explore a variety of rodent stress models and discuss the elements that influence the metabolic outcome in order to further extend our understanding of stress-induced obesity.

Cannabis is a commonly used substance among university students that may have several negative health repercussions, including suicidal ideation (SI) and suicide attempts (SA). The factors that contribute to or help explain this relation remain uncertain. Earlier negative experiences, especially trauma encountered during early life, have been associated with the development of psychopathology upon later stressor encounters. In the current study, we examined the associations between SI and SA with problematic cannabis use among young adults and the role of earlier trauma experiences and trait impulsiveness in understanding this link. Among university students (N = 539), problematic cannabis use was moderately related to lifetime and past-12-months suicidal ideation and attempts. Impulsiveness mediated the relationship between problematic cannabis use and lifetime SI and SA. Moreover, previous life trauma moderated the relationship between problematic cannabis use and SA, such that the association between problematic cannabis use and SA was stronger among those who experienced high levels of trauma. These findings highlight behavioral and environmental factors that could predict suicide ideation and attempts among young cannabis users. Accordingly, trait impulsiveness and early trauma experiences should be considered, alongside problematic cannabis use, in suicide-risk detection and prevention strategies among young adults.