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Research to effectively model rotational traumatic brain injury and discover potential neuroprotective therapies

Research to effectively model rotational traumatic brain injury and discover potential neuroprotective therapies

 


Dr. James A. Bibb’s lab has published its findings in the journal Scientific Reports.

Each year, millions of people worldwide suffer traumatic brain injuries (TBI). Caused by external forces such as a blow to the head that disrupt normal brain function, TBI can often result in a range of symptoms after the injury. Many patients report headaches, memory loss, poor concentration and attention, mood changes, and even sleep disturbances.

“These symptoms can be incredibly disruptive to a person’s daily life and can lead to poor quality of life, job difficulties, and strained relationships with loved ones.” Dr. James A. BibbChair of the University of Arizona School of Medicine-Phoenix Translational Neuroscience Division.

Division of Translational Neuroscience Advances New Models, Causes, and Treatments for the Most Serious Forms of Head Injury
Division of Translational Neuroscience Advances New Models, Causes, and Treatments for Most Severe Head Injuries

Despite the prevalence of TBI, available treatment options are limited. And most treatments now focus on managing symptoms rather than addressing the underlying damage. We attribute this to a lack of understanding of how it affects us.

Most TBI are the result of a fall, car accident, or sports-related head injury, in which the brain is damaged by rapid acceleration/deceleration of the brain within the skull. It’s very difficult to reproduce. “Few preclinical models of TBI replicate these negative rotational injuries, which makes it difficult to study the effects of TBI and test potential therapeutics in a controlled environment.” ‘he says Dr. Bibb.

However, a recent study by Umfress et al. al — was announced in scientific report Conducted in Dr. Bibb’s lab — highlighting the development of a new model of TBI induced by rotational acceleration.

Using complex mechanical engineering and high-speed telemetry, Dr. Bibb and his colleagues were able to design and characterize this new model. This has revealed many neuropathological consequences of injury.

Researchers used translational in vivo imaging of resident immune cells to demonstrate diffuse neuroinflammation after rotational head injury. Also, in partnership with Cell Signaling Technology, we utilized proteomic strategies to identify cyclin-dependent kinase 5 (Cdk5) as the primary culprit in his TBI-induced memory impairment.

They combined this with a novel inhibitor of Cdk5 (also discovered in Dr. Bibb’s lab) to demonstrate neuroprotection against these memory deficits and other neuropathological changes. Their progress provides fundamental steps towards modeling clinically relevant forms of TBI, identifying biochemical changes in the brain, and developing new neuroprotective therapeutics.

“The chronic effects of TBI include an increased risk of developing neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. It can lead to degenerative disease, which is a common condition in professional football players and other contact sports athletes,” explained Dr. Bibb. It is important for researchers to develop more effective treatments.

This multicenter study includes the Eric Jonson School of Engineering and Computer Science at the University of Texas at Dallas, the University of Texas Southwestern, the University of Alabama at Birmingham, Cell Signaling Technology, and the UArisona College of Medicine – Phoenix Department of Translational Neuroscience.

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