FELIX P. ECKENSTEIN
Professor
Neurology and
Anatomy and Neurobiology
Ph.D., Biozentrum, University of Basel, Switzerland, 1982
Postdoctoral training, Harvard Medical School
Nerve regeneration is regulated by specific cues present in the environment of injured neurons. What is the precise molecular nature of these cues and how do they signal the injured neuron to regenerate? To address these questions we are taking a multidisciplinary approach, ranging from molecular biology, to animal studies involving genetically modified mice. Our past work indicates that growth factors, such as FGFs, and cytokines, such as CNTF, play an important role in neuronal survival and regeneration after injury.
We now are defining the precise role of several members of the FGF family and CNTF by studying nerve injury in FGF and CNTF knockout mice. In addition, we are defining the intracellular targets of FGF signaling in injured neurons, using genetically modified FGF receptors in both cell culture models of neurite outgrowth and in transgenic mice.
Through collaborative efforts with other groups we study whether FGFs and CNTF are important in limiting damage after spinal cord injury and in preventing neurodegenerative diseases, such as Parkinson's and Alzheimer's disease.
Eckenstein FP, McGovern T, Kern D, Deignan J. (2006). Neuronal vulnerability in transgenic mice expressing an inducible dominant-negative FGF receptor. Exp Neurol.
198(2):338-49. 
Quinn J, Montine T, Morrow J, Woodward WR, Kulhanek D, Eckenstein F. (2003). Inflammation and cerebral amyloidosis are disconnected in an animal model of Alzheimer's disease. J Neuroimmunol.
137(1-2):32-41.
Stackman RW, Eckenstein F, Frei B, Kulhanek D, Nowlin J, Quinn JF. (2003). Prevention of age-related spatial memory deficits in a transgenic mouse model of Alzheimer's disease by chronic Ginkgo biloba treatment. Exp Neurol.
184(1):510-20.
Montine K.S., Montine T.J., Morrow J.D., Frei B., Milatovic D., Eckenstein
F., and Quinn J.F. (2002). Mouse cerebral prostaglandins, but not oxidative
damage, change with age and are responsive to indomethacin treatment.
Brain Res. 930: 75-82.
Quinn J., Davis, F., Woodward W.R., and Eckenstein, F. (2001). Beta-amyloid
plaques induce neuritic dystrophy of nitric oxide-producing neurons in
a transgenic mouse model of Alzheimer's disease. Exp. Neurol.168:
203-12.
Sheu J.Y., Kulhanek D.J., and Eckenstein F.P. (2000). Differential patterns
of ERK and STAT3 phosphorylation after sciatic nerve transection in the
rat. Exp. Neurol. 166: 392-402.
Clark W.M., Rinker L.G., Lessov N.S., Hazel K., Hill J.K., Stenzel-Poore
M., and Eckenstein F. (2000). Lack of interleukin-6 expression is not
protective against focal central nervous system ischemia. Stroke
31: 1715-20.
Kuzis K., Coffin J.D., and Eckenstein F.P. (1999). Time course and age
dependence of motor neuron death following facial nerve crush injury:
role of fibroblast growth factor. Exp. Neurol. 157: 77-87.
