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The Role of Brain-Lung Dysfunction in the Progression of Alzheimer’s Disease After Blast-induced Traumatic Brain Injury
Location: East Ballroom
Mentor: Dr. Nadine Kerr
Traumatic brain injury (TBI), defined as a sudden injury to the brain caused by an impact to the head, afflicts more than 5.3 Americans annually. Blast TBI, a form of traumatic brain injury, is caused by the overpressurization shock wave produced by high-energy explosives that directly impacts the skull and body, deeming it a blast injury to the body, including organs such as the lungs. Prior research suggests that lung injuries that compromise oxygenation can induce neuronal changes, highlighting the brain-lung axis connection. Research shows that nearly 25% of people who sustain a Traumatic Brain Injury (TBI) suffer from respiratory issues such as Acute Lung Injury (ALI). TBI-induced ALI has also been related to the regulation of the neural-respiratory-inflammasome axis. Previous studies in our laboratory have also found that TBI subjects predisposed to Alzheimer's Disease show increased inflammasome expression along with AD proteins. Moreover, respiratory diseases are the cause of death in 45% of patients with AD, compared to only 7% in the general population of a similar age, showing that there is a possible relationship between AD pathology and lung dysfunction as well. This study assessed the role of the systemic inflammatory response in brain-lung axis dysfunction in mice genetically predisposed to AD after Blast TBI. Following blast exposures, cortical and lung tissue was collected 24 hours and 56 days post-injury to assess acute injury through western blot protein analysis and chronic injury through histological analyses and lung injury scoring. The results highlight the increase in inflammasome and AD protein expression immediately following blast injury, in addition to the sustained presence of inflammatory markers, ASC and SPC in the lungs and Iba-1 in the cortex, in chronic cortical and lung samples. The results further depict the worsened lung pathology and chronic emphysema following blast injury, emphasizing the role of the systemic inflammatory response in brain-lung axis dysfunction in blast-injured mice predisposed to AD.
