Microglia dynamics in adolescent traumatic brain injury
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(2020) 17:326
REVIEW
Open Access
Microglia dynamics in adolescent traumatic brain injury Eric Eyolfson1,2,3, Asher Khan2,3, Richelle Mychasiuk1,2,3,4 and Alexander W. Lohman2,3,5*
Abstract Repetitive, mild traumatic brain injuries (RmTBIs) are increasingly common in adolescents and encompass one of the largest neurological health concerns in the world. Adolescence is a critical period for brain development where RmTBIs can substantially impact neurodevelopmental trajectories and life-long neurological health. Our current understanding of RmTBI pathophysiology suggests key roles for neuroinflammation in negatively regulating neural health and function. Microglia, the brain’s resident immune population, play important roles in brain development by regulating neuronal number, and synapse formation and elimination. In response to injury, microglia activate to inflammatory phenotypes that may detract from these normal homeostatic, physiological, and developmental roles. To date, however, little is known regarding the impact of RmTBIs on microglia function during adolescent brain development. This review details key concepts surrounding RmTBI pathophysiology, adolescent brain development, and microglia dynamics in the developing brain and in response to injury, in an effort to formulate a hypothesis on how the intersection of these processes may modify long-term trajectories. Keywords: Synaptic pruning, Glia, Pathophysiology, White matter, Brain maturation, Complement cascade
Background Traumatic brain injuries (TBI) can have devastating consequences on brain and mental health. Between Canada, the USA, and the European Union (EU), there are an estimated 46 million new TBI cases each year [1]. Among these, the vast majority (~ 80%) are classified as mild (mTBI) [2]. The highest age-specific rates for mTBI occurs in adolescents due to increased risk-taking behaviors and participation in contact sports [3], with sports-related mTBIs accounting for ~ 60% of all adolescent cases [4]. Importantly, individuals who sustain a single mTBI are at high risk for acquiring repetitive mTBIs (RmTBI) [5]. While preventative measures to reduce injury rates are improving, the incidence of adolescent RmTBI continues to grow with no current therapies to improve outcomes [6]. * Correspondence: [email protected] 2 Hotchkiss Brain Institute, University of Calgary, 3330 Hospital Drive NW, Calgary, AB T2N4N1, Canada 3 Alberta Children’s Hospital Research Institute, University of Calgary, 3330 Hospital Drive, NW, Calgary, AB T2N4N1, Canada Full list of author information is available at the end of the article
TBI pathophysiology encompasses primary and secondary injury cascades that collectively drive acute and chronic neurological damage and dysfunction. Defining the mechanisms of primary injury has been a major research focus, but the potential therapeutic window for intervention at this stage is limited, specifically in the case of mTBIs. This is because primary injury cascades initiate immediately following head trauma and unlike m
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