Identification of Immune Mechanisms of Traumatic Brain Injury-Induced Memory Decline
Can we reverse trauma-related deficits?
Each year in the United States, at least 2.5 million people suffer from traumatic brain injury (TBI). Elderly individuals are particularly vulnerable to TBI accounting for 22% of these injuries or 550,000 cases. Starting at age 65, the incidence of TBI doubles every 10 years. Elderly patients have clinically worse outcomes after TBI with enhanced morbidity, increased mortality, and exacerbated cognitive deficits including development of Alzheimer’s disease (AD). Despite the growing numbers of elderly individuals impacted by TBI limited studies investigate mechanisms for trauma-induced cognitive outcomes in an aging paradigm. Neuroinflammation is one potential mechanism for long-term cognitive deficits following TBI. Neuroinflammation refers to the activation of brain immune cells (microglia) and/or infiltration of peripheral immune cells (neutrophils, monocytes, T cells) into the brain parenchyma. Initially after trauma, these immune cells are important for debris clearance, however if left unchecked immune cells can damage neurons leading to cognitive decline (memory loss). Thus, determining the balance between a healthful and harmful immune state is imperative. This project focuses on understanding trauma-induced immune mechanisms, with a focus on investigating how age impacts these responses. The overall goal is to understand TBI-induced immune response(s) in an effort to develop effective treatment strategies to preserve cognitive functions in the aging brain.
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