Chapters authored
Age-Dependent Responses Following Traumatic Brain Injury
Traumatic brain injury (TBI) is a growing health concern worldwide that affects a broad range of the population. As TBI is the leading cause of disability and mortality in children, several preclinical models have been developed using rodents at a variety of different ages; however, key brain maturation events are overlooked that leave some age groups more or less vulnerable to injury. Thus, there has been a large emphasis on producing relevant animal models to elucidate molecular pathways that could be of therapeutic potential to help limit neuronal injury and improve behavioral outcome. TBI involves a host of different biochemical events, including disruption of the cerebral vasculature and breakdown of the blood-brain barrier (BBB) that exacerbates secondary injuries. A better understanding of age-related mechanism(s) underlying brain injury will aid in establishing more effective treatment strategies aimed at improving restoration and preventing further neuronal loss. This review looks at studies that focus on modeling the adolescent population and highlights the importance of individualized aged therapeutics to TBI.
Part of the book: Traumatic Brain Injury
Peripheral Immune Response Following Traumatic Brain Injury
Traumatic brain injury (TBI) represents a leading contributor to long-term neurological damage. Though TBI is a leading cause of death and neurological damage worldwide, there exists no therapeutic treatments to alleviate deleterious secondary injury due to neuroinflammation. The continuum of pro- and anti-inflammatory response elicited by TBI is suggested to play a key role in the outcome of TBI; however, the underlying mechanisms remain poorly defined. This chapter explores rodent models of injury used to study the disease pathology of TBI, as well as the major contributions of the peripheral immune response following injury. Further, this chapter discusses the influence of individual immune cell types on neuroinflammation following TBI, focusing on peripheral monocyte/macrophages, their polarization state, and the current literature surrounding their behavior within the TBI milieu. Finally, cell-to-cell contact regulators that effect peripheral-induced neuroinflammation and may serve as novel targets for therapeutics will be highlighted.
Part of the book: Advancement and New Understanding in Brain Injury