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Probing the Mechanistic Role of Vascular Dysfunction and Vascular Inflammation in TBI-Mediated Cognitive Dysfunction

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Technical Report,01 Aug 2018,31 Jul 2019

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Carl T. Hayden Medical Research Foundation Phoenix United States

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Traumatic brain injury TBI is a major cause of mortalitymorbidity among service-membersveterans and is linked to long-term development of aging related dementia disorders through still poorly-defined mechanisms. We are testing the hypothesis that an important etiopathologic basis of TBI-related cognitive dysfunction is cerebrovascular dysfunction and vascular inflammation resulting in chronic brain hypoperfusion. We are also testing the hypothesis that TBI confers susceptibility to later development of cardiovascular risk factorspecifically diabeteshyperglycemia-related cerebrovascular dysfunction leading to cognitive impairment. In Aim 1 we will measure the cognitive function of Sprague-Dawley rats exposed to TBI by fluid percussion injury and determine the relationship with cerebrovascular function in vivo by MRI and ex vivo by circle of Willis artery vasoreactivity and vascular inflammation. In Aim 2 we will determine whether TBI and diabetes-related metabolic derangements or -amyloid confer synergistic deleterious effects on cognitive function, cerebrovascular function and inflammation. We completed the cohorts who underwent injury or sham treatment and obtained 6-month cognitive function and in-vivo and ex-vivo cerebrovascular function data, but our data remains preliminary and incomplete. Preliminary data so far show impaired cognitive function 6 months following TBI with some regional association between cognitive and in vivo cerebrovascular function, but we advise caution in interpretation due to incomplete data.

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  • Anatomy and Physiology

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