Research  |  Core Facilities  |  Patient Studies  |  Tech Transfer  |  Seminars  |  Intranet  |  Jobs  |  Search  |  Contact Us  |  Ways To Give                             HOME

More about
Dr. Hensley:

Dr. Hensley 101
(for non-scientists)

Dr. Hensley's CV in brief

Publications

Free Radical Biology and Aging Research Program

Kenneth Hensley, Ph.D. Associate Member, Free Radical Biology and Aging Research Program

Research Interests
My laboratory studies the process of neuro-inflammation, a specific type of innate immune response that occurs in the brain during many, and perhaps all, neurodegenerative diseases (including Alzheimer’s, Parkinson’s, Huntington’s and various motor neuron diseases). Neuroinflammation is manifested by activation of microglial cells in response to dysregulated cytokine networks and may be triggered by deposits of toxic protein or dead cell debris. For instance, amyloid peptides trigger a neuroinflammatory reaction in the Alzheimer’s disease-afflicted brain. Other proteins are implicated in other diseases, and different brain regions are affected, but the biochemical principles are very similar. Normally, microglia remove dead cells and pre-cancerous cells, but when triggered into a neuroinflammatory state, the microglia attack neurons either directly or through “collateral damage.” The activated microglia release a host of toxic agents, especially free radicals (such as nitric oxide), that severely interfere with healthy neuron function.

Our main tool for studying neuroinflammation is the G93A-SOD1 transgenic mouse, which carries the human gene mutation responsible for hereditary amyotrophic lateral sclerosis (ALS, or Lou Gehrig’s disease). In this animal, the motor neurons of the brain and spinal cord deteriorate at three to four months of age, and the mouse becomes paralyzed. We have developed a model in which a cytokine (TNF) drives the neuroinflammatory reaction. We have established a cell culture screen for inhibitors of this process, and we have identified several classes of natural compound that block TNF activation of microglia. We are currently evaluating these agents in the ALS mouse and are extending our findings to other systems, most notably Huntington’s disease, where appropriate animal genetic models exist.

Another very new project in my laboratory focuses on exploring the role of mitochondria (cell energy-producing organelles) in promoting neuroinflammation by affecting cellular signal transduction within the glial cells of the brain.

Joined OMRF Scientific Staff in 1996.

Mailing Address
Free Radical Biology and Aging Research Program, MS 21
Oklahoma Medical Research Foundation
825 N.E. 13th Street
Oklahoma City, Oklahoma 73104

Contact Information
Phone: (405) 271-7569
Fax: (405) 271-1795
E-mail: Kenneth-Hensley@omrf.org