Faculty Detail   
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Graduate Biomedical Sciences Affiliations
Cell, Molecular, & Developmental Biology 
Cellular and Molecular Biology Program 
Neuroscience 
Neuroscience Graduate Program 
Pathobiology and Molecular Medicine 

Biographical Sketch 
James Madison University, B.A. 1991
Virginia Commonwealth University, M.S. 1998
Virginia Commonwealth University, Ph.D. 2000
University of California, Davis Post-doc 2001-2004


Faculty Positions:
2004- 2006 Assistant Professor, Department of Neurosurgery, University of California, Davis.

2006- 2012 Assistant Professor, Department of Physical Medicine and Rehabilitation, University of Alabama at Birmingham.

2012-current Associate Professor and Director of Research, Department of Physical Medicine and Rehabilitation, University of Alabama at Birmingham

Candace L. Floyd, Ph.D., received her M.S. from Medical College of Virginia/Virginia Commonwealth University in 1998 where she studied traumatic brain injury using in vivo rodent models under the tutelage of Bruce G. Lyeth, Ph.D. She received her Ph.D. from the same institution in 2000, under the mentorship of Earl Ellis, Ph.D., and focused her research on in vitro mechanical strain injury in astrocytes. She conducted her post-doctoral training in traumatic CNS injury at the University of California, Davis from 2001-2004. In 2004, she became an Assistant Professor in the Department of Neurological Surgery at the University of California, Davis. In 2006, she moved to the University of Alabama at Birmingham, where she joined the Center for Glial Biology in Medicine and is an Assistant Professor in the Department of Physical Medicine and Rehabilitation. The central focus of her research is to understand glial-neuronal interactions in traumatic brain and spinal cord injury. Recent work from the Floyd laboratory evaluates the protective actions of 17b-estradiol in traumatic CNS injury. Other work evaluates bioengineering approaches to regeneration and repair. The Floyd lab also investigates glial-neuronal interactions in neuropathic pain after CNS injury. She has served as an invited instructor in the Reeve-Irvine Spinal Cord Injury Techniques Course, as an ad-hoc member of NIH study sections, and has also reviewed grant applications for the Department of Defense and the Veteran's Administration. She frequently reviews manuscripts for several neuroscience journals, including the Journal of Neurotrauma and is an active member of the National Neurotrauma Society.









Society Memberships
Organization Name Position Held Org Link
American Association for the Advancement of Science    http://www.aaas.org/ 
International Neurotrauma Socitey     
National Neurotrauma Society  Secretary-Treasurer, Vice-President  http://www.edc.gsph.pitt.edu/neurotrauma/index.html 
Society for Neuroscience  Program Committee  http://www.sfn.org/ 
 

Research/Clinical Interest
Title
Neuronal-Glial Interactions in Traumatic Brain and Spinal Cord Injury
Description
Millions of people a year suffer a traumatic brain or spinal cord injury (TBI or SCI); and in the blink of an eye, their lives may be changed forever. The current clinical repertoire for treating CNS injury is extremely limited. In fact, there are no pharmacological interventions to treat TBI and only one drug with questionable efficacy for use in SCI. Most previous research in CNS injury has focused on neuroprotection, and has discounted the role of glial cells in injury pathology. The central hypothesis of our research is that understanding of the complex interaction of glial and neuronal cells in the pathophysiology of traumatic CNS injury will lead to novel, effective therapeutic interventions. On-going projects include: a) estrogens, phytoestrogens, and selective estrogen receptor modulators (SERMs) as potential protective agents in TBI and SCI b) bioengineering approaches to promote regeneration and repair of the injured spinal cord c) mechanisms and implications of glial cell death in traumatic brain and spinal cord injury d) understanding neuronal-glial interactions in neuropathic pain after spinal cord injury e) elucidating pathological mechanisms underlying lasting cognitive deficits after mild TBI (concussion)

Selected Publications 
Roman JA, Niedzielko TL, Haddon RC, Parpura V, Floyd CL.
Single-walled carbon nanotubes chemically functionalized with polyethylene glycol promote tissue repair in a rat model of spinal cord injury.
J Neurotrauma. 2011 Nov;28(11):2349-62. Epub 2011 Apr 12. 
21303267 
Dunham KA, Siriphorn A, Chompoopong S, Floyd CL.
Characterization of a graded cervical hemicontusion spinal cord injury model in adult male rats.
J Neurotrauma. 2010 Nov;27(11):2091-106.
 
21087156 
Siriphorn A, Chompoopong S, Floyd CL.
17b-estradiol protects Schwann cells against H2O2-induced cytotoxicity and increases transplanted Schwann cell survival in a cervical hemicontusion spinal cord injury model.
J Neurochem. 2010 Nov;115(4):864-72.
 
20456002 
Olsen ML, Campbell SC, McFerrin MB, Floyd CL, Sontheimer H.
Spinal cord injury causes a wide-spread, persistent loss of Kir4.1 and glutamate transporter 1: benefit of 17 beta-oestradiol treatment.
Brain. 2010 Apr;133(Pt 4):1013-25.
 
20375134 
Kachadroka S, Hall AM, Niedzielko TL, Chongthammakun S, Floyd CL.
Effect of endogenous androgens on 17beta-estradiol-mediated protection after spinal cord injury in male rats.
J Neurotrauma. 2010 Mar;27(3):611-26.
 
20001688  
 

Keywords
spinal cord injury, traumatic brain injury, rat, mouse, astrocyte, protection, neuroprotection, pain