The Role of Inflammation in development of Alzheimers disease following repetitive head trauma
Technical Report,01 Aug 2017,31 Jul 2018
Indiana University School of Medicine Indianapolis United States
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Traumatic brain injury TBI affects approximately 3.8 million people annually and costs the US more than 48 million. Furthermore, TBI hasbecome an increasingly common feature of modern military conflicts. It has been estimated that in the Iraq and Afghanistan conflictsfollowing the terrorist attacks of September 11, 2001, the rate of TBI in military populations has dramatically increased to upwards of 10-20of those serving, with over 250,000 soldiers exposed to some form of TBI Source DoD. The long-term consequences of TBI aremultifaceted and include increased risk for AD. To date, mechanisms linking TBI to AD remain unclear. One of the earliest hallmark featuresof TBI is neuroinflammation, which is defined as the brains innate immune response. Post-injury neuroinflammation includes activation ofbrain resident microglia, infiltration of peripheral monocytes due to disruption of the blood-brain barrier, and high level production of pro- and anti-inflammatory molecules. Although this initial response is thought to promote repair following TBI, exaggerated or persistentneuroinflammation can be detrimental. For example, TBI can trigger progressive neurodegneration, brain atrophy, neuronal loss, and axonaldegeneration for months to years after the initial insult and these events are often associated with neuroinflammation. We hypothesize thatthe TBI-induced neuroinflammatory response is critical in mediating AD-related pathology and specific inflammatory proteins can be used aspost-injury biomarkers.
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