%0 Journal Article
%T Traumatic Brain Injury, Microglia, and Beta Amyloid
%A Rebekah C. Mannix
%A Michael J. Whalen
%J International Journal of Alzheimer's Disease
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/608732
%X Recently, there has been growing interest in the association between traumatic brain injury (TBI) and Alzheimer¡¯s Disease (AD). TBI and AD share many pathologic features including chronic inflammation and the accumulation of beta amyloid (A¦Â). Data from both AD and TBI studies suggest that microglia play a central role in A¦Â accumulation after TBI. This paper focuses on the current research on the role of microglia response to A¦Â after TBI. 1. Introduction Recently, there has been growing interest in the association between traumatic brain injury (TBI) and Alzheimer¡¯s Disease (AD). The interest grew from several lines of evidence, including epidemiological studies that demonstrated an association of TBI and the development of AD later in life [1¨C7] and autopsy studies that showed acute and chronic AD-like pathology in TBI victims [8, 9]. While most of the studies investigating the association of AD and TBI have focused on the accumulation and clearance amyloid-¦Â (A¦Â) [2, 8, 9], chronic neuroinflammation is also a common feature of AD and TBI, and microglia likely play a central role [10, 11]. In AD, microglia are recruited to newly formed A¦Â plaques, where microglial activation functions as a double-edged sword, promoting beneficial responses such as A¦Â clearance [12¨C14] while also eliciting a proinflammatory response [12]. Similar patterns of microglia activation have been demonstrated both acutely and chronically after TBI [15, 16]. This paper will explore the current research on the role of microglia response to A¦Â after TBI. Although there are few studies that directly examine microglial reaction to trauma-induced A¦Â, data from TBI and AD experimental and human studies will be used to make an argument for a central role of microglia in acute and chronic responses to A¦Â-mediated secondary injury after TBI. 2. General Microglial Response after TBI TBI is a disease process in which mechanical injury initiates cellular and biochemical changes that perpetuate neuronal injury and death over time, a process known as secondary injury. Secondary injury begins minutes after injury and can continue years after the initial insult. Mechanisms implicated in secondary injury after TBI include glutamate excitotoxicity, blood-brain barrier disruption, secondary hemorrhage, ischemia, mitochondrial dysfunction, apoptotic and necrotic cell death, and inflammation [17]. As the primary mediators of the brain¡¯s innate immune response to infection, injury, and disease, microglia react to injury within minutes. In fact, microglia may represent the first line of defense
%U http://www.hindawi.com/journals/ijad/2012/608732/