Download TBI Abstract - Stacey Lee, PhD

yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project

Document related concepts

Brain wikipedia, lookup

Psychoneuroimmunology wikipedia, lookup

Intracranial pressure wikipedia, lookup

Neuroeconomics wikipedia, lookup

Subventricular zone wikipedia, lookup

Nervous system network models wikipedia, lookup

Biochemistry of Alzheimer's disease wikipedia, lookup

Human brain wikipedia, lookup

Neuroinformatics wikipedia, lookup

Neurophilosophy wikipedia, lookup

Cognitive neuroscience wikipedia, lookup

Brain morphometry wikipedia, lookup

Molecular neuroscience wikipedia, lookup

Blood–brain barrier wikipedia, lookup

Connectome wikipedia, lookup

Holonomic brain theory wikipedia, lookup

Neurolinguistics wikipedia, lookup

Selfish brain theory wikipedia, lookup

History of neuroimaging wikipedia, lookup

Activity-dependent plasticity wikipedia, lookup

Neuroregeneration wikipedia, lookup

Brain Rules wikipedia, lookup

Aging brain wikipedia, lookup

Neuroanatomy wikipedia, lookup

Neuropsychology wikipedia, lookup

Clinical neurochemistry wikipedia, lookup

Neuroplasticity wikipedia, lookup

Haemodynamic response wikipedia, lookup

Metastability in the brain wikipedia, lookup

Neuropsychopharmacology wikipedia, lookup

Traumatic brain injury wikipedia, lookup

Stacey Lee, PhD and Jim Lechleiter, PhD
Department of Cellular and Structural Biology, UTHSCSA
Traumatic brain injuries (TBIs) are the cause of over 30% of injury-related deaths
in the United States. Both civilians and military personnel are at risk for TBIs from blunt
force or blast trauma. Side effects of TBI can range from dizziness, nausea, headaches,
concentration problems, memory impairment, mood disorders, and seizures. On a
molecular level, there are two phases of injury after a TBI. The primary phase is the
initial physical trauma. The secondary phase occurs within the following days of the
injury leading to edema, excitotoxicity, neuronal damage, cell death, inflammatory
responses, and blood-brain barrier dysfunction. Currently, there is no FDA-approved
treatment for TBI despite an urgent need for one. The goal of our work is to characterize
novel therapeutic compounds to mitigate brain damage induced by TBI. The project
aims to mitigate injury responses by improving astrocyte energy metabolism.
Astrocytes are essential for maintaining neuronal function and homeostasis in the
brain. They provide neurons with metabolic support, modulate synaptic transmission,
and aid in repair after injury. Previous research from the lab has shown that enhancing
mitochondrial metabolism in astrocytes protects neurons from oxidative stress.
Specifically, treating astrocytes with a purinergic receptor agonist enhances their ATP
production and decreases cytotoxic edema and reactive gliosis. We hypothesize that
enhancing astrocyte metabolic activity with these agonists will protect the brain against
TBI-induced damage.
We have two mechanisms for generating TBIs: a pneumatic impact device that
generates a closed controlled cortical impact, or blunt trauma, and an air-driven shock
tube simulating an IED explosion, or blast trauma. Using these two methods, we will
asses the ability of our compounds to reduce astrocyte injury response, injury size,
edema, inflammatory response, behavior, and seizures. We predict agonist treatment
after injury will prevent the secondary damage responses from exacerbating the injury
and lead to an improved outcome on a molecular and behavioral level. This work is
supported by the Department of Defense grant number W81XWH-15-1-0283.