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Funded Projects

Along with the generous support of donors, the Brain Injury Association of America is committed to finding cures for brain injury.

2021 Awards

“The Effects of Early Life Stress on Outcome after Mild Traumatic Brain Injury”
Seed Grant of $25,000
Grantee: Dr. Colleen Atkins, Ph.D., University of Miami Miller School of Medicine

Mild traumatic brain injury (mTBI) is a significant health problem in the US. Although most people with mTBI recover within a few weeks, a subset have persistent symptoms. The factors that contribute to persistent symptoms after mTBI are unknown. One potential factor identified in a study of mTBI patients is pre-exposure to stress in early development. Early life stress is highly prevalent and causes immune dysregulation in adulthood. This proposal will determine if early life stress limits recovery after a mTBI and test if an anti-inflammatory drug improves recovery after mTBI and stress.

“Analyses of the Relationship between Growth Hormone and Sleep after Pediatric Traumatic Brain Injury”
Seed Grant of $25,000 supported by Chaikin, Sherman, Cammarata & Siegel, P.C.
Grantee: J Bryce Ortiz, Ph.D., University of Arizona College of Medicine – Phoenix
Mentor: Rachel Rowe, Ph.D.

Traumatic brain injury (TBI) can lead to dysfunctions of the growth hormone (GH) axis and disrupt the sleep-wake cycle in children. Here, using advanced biological, analytical, and statistical methods, we will determine the relationship between the GH-axis and the sleep-wake cycle using a pediatric TBI animal model. We will also determine how hypothalamic nuclei that control the GH-axis are changed following TBI. These studies will inform us of novel research directions and potential treatments to help treat and care for pediatric TBI survivors.

“Pediatric TBI Effects on Long-term Myelination: Sex Specificity and Neuroimmune Modulation”
Seed Grant of $25,000
Grantee: Kathryn Lenz, Ph.D., The Ohio State University (Psychology)
Mentor: Jonathan Godbout, Ph.D.

Traumatic brain injury (TBI) is the leading cause of pediatric emergency room visits. Boys are more likely than girls to experience early-childhood TBI, which can lead to sex-specific risks for subsequent psychiatric disorders. Neuroimmune cells mediate healthy brain development, are sexually dimorphic, and their function is perturbed by TBI. Using a preclinical rat model of TBI, we will assess sex-specific inflammatory function and determine how brain myelination and motivated behavior are impacted, to discover new potential strategies to treat or prevent long-term outcomes of childhood TBI.

“The Role of FK506-binding Protein 51 (FKBP5) in Long-term Psychosocial Outcomes of Pediatric TBI”
Dissertation Grant of $5,000 supported by Dr. Lance and Laura Trexler
Grantee: Dana Lengel, Drexel University
Mentor: Ramesh Raghupathi, Ph.D.

Childhood Traumatic Brain Injury (TBI) results in increased risk for psychosocial disorders that can emerge in adolescence and adulthood. This vulnerability may be due to the susceptibility of developing neural stress circuits to TBI. In this proposal, we investigate the role of FK506-binding protein 51 (FKBP5), a co-chaperone of the glucocorticoid receptor (GR) and psychiatric risk factor, in behavioral and neuroendocrine effects of social stress following pediatric TBI. Targeting the GR system through FKBP5 may be able to mitigate the risk for psychosocial disorders following childhood TBI.

2020 Awards

“Meningeal and Trigeminal Contributions to Post-TBI Pain” 
Seed Grant of $25,000
Grantee: Orion Furmanski, Ph.D., Uniformed Services University (Dept. of Anatomy, Physiology, and Genetics)
Mentor: David Mears, Ph.D.

Posttraumatic headache (PTH) is characterized by increased headache frequency and/or severity following a traumatic brain injury (TBI). Current treatments for headache often fail to provide adequate relief for PTH. Improving treatment for PTH has been hindered by lack of knowledge on how TBI alters the nervous system to cause chronic headaches. We propose preclinical experiments to examine TBI effects on nerves of the dura mater, the protective jacket between the brain and skull. We hypothesize that dura mater injury promotes inflammation and abnormal pain processing that contribute to PTH.  

“The Epidemiology of Comorbidities and Associations with Functional Outcome among Adults with TBI.”
Seed Grant of $24,893
Grantee: Raj Kumar, Ph.D., Icahn School of Medicine at Mount Sinai (Rehabilitation and Human Performance)                 
Mentor: Kristen Dams-O’Connor, Ph.D.

As rates of traumatic brain injuries (TBI) increase and the population ages, there is an unprecedented urgency to understand the burden and implications of health morbidity on TBI recovery. Prior TBI studies are limited by incomplete disease characterization and under-representation of older adults, necessitating use of population-based data. Existing indices focus on predicting acute mortality (not function) and exclude diseases associated with TBI. We propose: 1) to use an administrative dataset to characterize disease prevalence, and 2) to create a functionally-relevant comorbidity index. 

“Precision identification and targeting of rod microglia in diffuse brain-injured cortex”
Dissertation Award of $5,000
Grantee: Katherine Giordano, University of Arizona College of Medicine (Child Health)
Mentor: Jonathan Lifshitz, Ph.D.

Neurological insults, such as traumatic brain injury, trigger inflammation signaling that go on to activate microglial cells. In this proposal, we investigate lesser-known microglia subtype, the rod microglia, to determine cell surface markers and gene expression unique to their occurrence after diffuse traumatic brain injury. These rod microglia markers could serve as biomarkers in the diagnosis and prognosis of injury and recovery from neurological injury.

“Impact of Intestinal Inflammation on Long-Term Neurological Outcomes Following TBI in Mice”
Dissertation Award of $5,000
Grantee: Marie Hanscom, University of Maryland-Baltimore (STAR-ORC)
Mentor: Terez Shea-Donohue, Ph.D.

Traumatic brain injury (TBI) causes peripheral organ dysfunction including gastrointestinal dysfunction. Increased gut leakiness is associated with greater risk of comorbidities in trauma patients. TBI patients surviving longer than 1-year post-injury are more likely to die of sepsis and digestive conditions. Infection with an intestinal pathogen in mice worsened TBI lesion volume. This study examines the effect of intestinal inflammation following TBI on long-term TBI-associated brain injury, inflammation and cognitive dysfunction and the role of the brain-gut axis in TBI disease progression.

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For many people, brain injury evolves into a chronic health condition that can cause or accelerate multiple diseases. Through BIAA's Redmann Research Program, we are determined to find a cure for brain injury.

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