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Home > Our Research Faculty > John Bethea, Ph.D.

 

JOHN R. BETHEA, PH.D.

Associate Professor, Departments of Microbiology and Immunology and Neurological Surgery

 

 

Immunological Consequences of SCI and The Development of Neuroprotective Strategies

 

Research Interests

John R. Bethea, Ph.D.

 

In my laboratory we are studying spinal cord injury (SCI) and diseases of the nervous system such as Multiple Sclerosis (MS) to try to understand the cellular and molecular mechanisms that contribute to astrogliosis and secondary neuronal cell death. To this end, my laboratory has two main research objectives. First, we are studying the neuro-inflammatory response that occurs following SCI and secondly, develop novel therapies for SCI and diseases of the central nervous system.

To determine what role(s) trauma-induced inflammation plays in mediating secondary neuronal injury and cell death following SCI, we use transgenic mouse models and other molecular biological approaches. We have recently demonstrated that traumatic SCI initiates a very robust inflammatory response, both within the spinal cord and systemically. Specifically, we have shown that traumatic SCI activates NF-kB within macrophages, microglia, endothelial cells and neurons. NF-kB is a transcription factor that plays a pivotal role in regulating inflammation, and possibly apoptotic cell death pathways. We have recently generated mice that do not express functionally active NF-kB in astrocytes and have determined that these mice are significantly protected from SCI and MS-induced paralysis, inflammation and myelin damage.

The second major focus of my laboratory is to develop neuroprotective strategies for the treatment of acute SCI and MS. To this end, performing high-content screening assays to try and identify novel regulators of NF-kB activation and astrogliosis. The goal of these studies is to identify novel inhibitors of NF-kB activation in astrocytes and test the neuroprotective potential in animal models of SCI and MS.

 

 

 

 

 
 
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