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Neurology Translational Research

The Barrow Neurological Institute at Phoenix Children’s recognizes that excellence in clinical care is interdependent with excellence in research. In order to diagnose, treat and prevent neurological diseases and disorders, we need an extensive base of knowledge. This knowledge is gained through medical research. Basic research is research that happens in the laboratory. To continually improve care, we have three research laboratories: epileptogenesis, neurotrauma and neuro-oncology.

Translational basic researchers evaluate the nature of circuit alterations that underlie acute neurological conditions. Researchers focus on the acute phase in which circuits are dismantled, followed by the chronic phase of circuit reorganization. By understanding the processes of circuit dismantling and reorganization, we can develop therapeutic interventions (pharmacological, rehabilitative, restorative and regenerative) to mitigate neurological conditions. 

Translational Neurotrauma Research Program

The Translational Neurotrauma Research Program, directed by Theresa Currier Thomas, PhD, is a multi-institutional collaboration representing the University of Arizona, College of Medicine – Phoenix, the Barrow Neurological Institute at Phoenix Children’s and the Phoenix Veterans Administration Health Care System.

We fulfill a critical component of the mission to improve the health and quality of lives of people (particularly children and veterans) living with acute neurological injuries, specifically traumatic brain injury. Laboratory and clinical research provide new knowledge into restorative and regenerative medicine that can advance clinical care and improve outcomes.

Research efforts in the Neurotrauma Research Program focus on restorative and regenerative treatments for acquired neurological conditions such as traumatic brain injury. In particular, scientific aims target circuit disruption contributing to lasting neurological symptoms.

In response to neurotrauma, brain circuits dismantle over a short period of time, due to mechanical forces and ensuing secondary activity. Thereafter, the brain repairs, rebuilds and reorganizes itself but not necessarily reconstituting the original template.

Instead, circuits can become rewired, thereby processing information differently. In this way, new neurological symptoms and morbidities emerge after acute neurological insults. Pharmacological and rehabilitative therapies can mitigate circuit dismantling and promote adaptive circuit reorganization, thereby preserving function and quality of life.

Active Projects in Translational Research

Our research strategies draw on clinical symptoms in need of new knowledge. Each strategy is matched between laboratory and clinical investigation to advance translational applications. We are working on identifying injury-induced morbidity, determining underlying causes and targeting therapy to specific treatable populations.

  • Sensory sensitivity leads to agitation and irritation to light and sound in people living with brain injury. Our diffuse brain injury model shows rodents develop sensory sensitivity to somatic whisker stimulation over one month post-injury. This morbidity correlates with plastic changes in the whisker circuit associated with synaptogenesis and inflammation. Our research investigates interventions to mitigate these processes in rodents, while imaging brain-injured patients with light sensitivity
  • Endocrine dysfunction can explain the range of metabolic and mood disorders evident in chronic brain injury survivors. Our brain-injured rodents show exacerbated endocrine levels to non-noxious stimulation and likely to other stressors, as anecdotally reported for brain injury survivors. Our research investigates avenues to alleviate or prevent endocrine dysfunction in rodents, while gathering prospective data and testing hormone replacement in veterans.
  • Aging with injury: TBI in adolescents causes long-term neurodegeneration that can lead to late-onset, persisting symptoms and increased risk for developing age-associated neurodegenerative disorders with varied sex-dependent outcomes. Our experimental model of diffuse TBI demonstrates that the chronic neurodegeneration is associated with region- and sex-dependent temporal profiles of glial activation between aging with injury and normal aging associated with the development and persistence of behavioral deficits that can interfere with neurodevelopmental milestones. 
  • Sex differences: Girls and women report a greater number, severity and duration of symptoms and are 50-75% more likely than males to suffer adverse reactions to drug therapy, yet are only included in 10% of preclinical TBI research. Our published and preliminary data demonstrate multiple novel sex differences in neurosynaptic activity, physiology and behavioral responses before and after TBI that may fundamentally impact the efficacy of drug therapies and circuit function.

The great challenge lies with mild TBI because, far too often, no medical advice is sought. Also, cognitive, neuroendocrine and mental health deficits can develop weeks to years post-injury, where a correlation between symptoms and the instigating TBI are not made, predominantly because the occurrence of a TBI is not a universal patient history question. This correlation is important for clinicians to consider alternate testing to identify the root cause of presenting symptoms and identify the optimal treatment. Knowledge gained from our clinical and translational collaborations is critical to guide clinical treatment algorithms for TBI patients, including long-term follow-up testing and overall improving outcomes in our patient population.

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