Kathryn J. Jones, Ph.D.

Professor

Department of Cell Biology, Neurobiology and Anatomy

B.S. and Certificate, Physical Therapy, 1975. University of Wisconsin-Madison.
Ph.D., Neuroscience, 1983. Department of Anatomy, University of Illinois at Chicago.
Postdoctoral Fellow, Neuroendocrinology, 1983-1986. Laboratories of Neurobiology and Behavior, and Neuroendocrinology, The Rockefeller University.

EMAIL

Current Interests

Gonadal steroid hormones as neurotherapeutics in PNS and CNS injuries, translational studies of gonadal steroid use in facial paralysis caused by acoustic neuromas, neuroimmunology and CD4+T-mediated neuroprotection, ALS and motoneuron diseases

Laboratory Focus

The overall goal of the research in our laboratory is to understand the basis for successful neuronal regeneration in neurons capable of survival and full axonal regrowth following injury and to extrapolate that information to enhance survival and regeneration of neurons otherwise incapable of survival and/or axonal regrowth and injury. We are currently investigating the use of steroids for the treatment of facial nerve paralysis induced by intracranial tumors.

 

Toward that goal, we have a number of currently funded projects which are focused on elucidating the cellular/molecular events associated with nerve regeneration. The therapeutic role of gonadal steroids in enhancing peripheral nerve is being investigated. Gonadal steroids are neurotrophic agents capable of affecting many neuronal properties associated with successful regeneration. In the human neurological disorder, amyotrophic lateral sclerosis, a steroid hormone receptor deficiency has been postulated to play an etiological role in the development of that disease. Administration of testosterone at the time of facial nerve injury in adult rodents accelerates functional recovery from facial paralysis. These steroidal effects on nerve regeneration are steroid receptor-mediated and appear to involve an augmentation of the intrinsic molecular program of regenerating facial neurons. We are also exploring the ability of steroids to improve outcome from spinal cord injury in rodent models. The long-term objective is to extend these studies to the human. In collaboration with Dr. Virginia Sanders, we have recently discovered a role for CD4+T cells in promoting motoneuron survival after peripheral nerve injury and have advanced a model for how motoneurons direct a pro-survival, anti-inflammatory injury response.  The long term goal of these studies is to extrapolate the results to ALS and other motoneuron diseases. 

Publications

Huppenbauer, C.B., Tanzer, L., DonCarlos, L.L., and Jones, K.J. (2005) Gonadal

steroid attenuation of developing hamster facial motoneuron loss by axotomy: equal

efficacy of testosterone, dihydrotestosterone, and 17-beta estradiol, J. Neurosci.,

25:4004-4013.

DeBoy, C.A., Byram, S.C., Serpe, C.J., and Sanders, V.M, and Jones, K.J. (2006)

 Immune-mediated neuroprotection of axotomized mouse facial motoneurons is

 dependent on the IL-4/STAT6 signaling pathway in CD4+ T cells, Exp. Neurol.,.

 201:2120224.

Tetzlaff, J.E., Huppenbauer, C.B., Tanzer, L., Alexander, T.D., and Jones, K.J.

 (2006) Motoneuron injury and repair: new perspectives on gonadal steroids as

 neurotherapeutics.  J. Molec. Neurosci, 28: in press.

Byram, S.C., Serpe, C.J., DeBoy, C.A., Sanders, V.M. and Jones, K.J. (2006) The

neuroprotective Th1/Th2 paradigm: a working model of motoneuron repair.  Clin.

 Neurosci. Res., 6: 86-96.