T. Bucky Jones, Ph.D.

My current projects are broadly aimed at determining the effects of the innate immune system response to CNS trauma or neurodegenerative disease in Drosophila melanogaster models of traumatic brain injury (TBI) or Parkinson's disease, respectively. Specifically, we are interested in defining more precisely the mechanisms by which reactive oxygen species (ROS), including nitric oxide (NO) influence functional outcomes following TBI or in the presence of PRKN ( parkin ) gene mutations.

My work in AD is designed to investigate the effects of infectious disease processes on AD pathology in post-mortem human brain tissues. This work is testing the overall hypothesis that chronic infection and concomitant inflammation in the brain that occurs as part of the host response to infection induces histopathological features characteristic of this neurodegenerative disorder.

My work in neurodegenerative disorders has significant overlap with my research in CNS trauma in which I have been involved since 2001. Many of the neuroinflammatory mechanisms that are present in AD and PD patients (i.e., changes in glial morphology and functional phenotype) are similar to inflammatory processes that occur following trauma and vascular injury to the CNS. These immune signaling pathways are evolutionarily conserved and homologous pathways are present in Drosophila . Thus, my newest work utilizing a Drosophila model will draw on my previous work but will allow us to investigate more fully, mechanisms that have not been able to be defined in more complex animals.

My primary research focus over the past 14 years has been in studying the role of neuroinflammation in recovery of function after spinal cord injury. My background in spinal cord trauma has provided me with extensive experience working with rats and mice, and in evaluating histological, morphological and functional characteristics of CNS-specific cells (e.g., microglia and lymphocytes).
Alzheimer's disease
Parkinson's disease
Traumatic Brain Injury