The Role of Inflammation in Development of Alzheimer's Disease Following Repetitive Head Trauma
Technical Report,01 Aug 2016,31 Jul 2017
Indiana University 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 has become an increasingly common feature of modern military conflicts. It has been estimated that in the Iraq and Afghanistan conflicts following the terrorist attacks of September 11, 2001, the rate of TBI in military populations has dramatically increased to upwards of 10-20 of those serving, with over 250,000 soldiers exposed to some form of TBI Source DoD. The long-term consequences of TBI are multifaceted and include increased risk for AD. To date, mechanisms linking TBI to AD remain unclear. One of the earliest hallmark features of TBI is neuroinflammation, which is defined as the brains innate immune response. Post-injury neuroinflammation includes activation of brain 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 persistent neuroinflammation can be detrimental. For example, TBI can trigger progressive neurodegeneration, brain atrophy, neuronal loss, and axonal degeneration for months to years after the initial insult and these events are often associated with neuroinflammation. We hypothesize that the TBI-induced neuroinflammatory response is critical in mediating AD-related pathology and specific inflammatory proteins can be used as post-injury biomarkers.
- Medicine and Medical Research
- Anatomy and Physiology
- Genetic Engineering and Molecular Biology