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John P. Crow, Ph.D.
Professor and Director, J. Thomas May Center for Amyotrophic Lateral Sclerosis Research

John P. Crow, Ph.D.
PHD
Auburn University, M.S., 1986, University of South Alabama, Ph.D., 1991

Research Interests
At present, we are focused primarily on identifying and characterizing new drug treatments for Amyotrophic Lateral Sclerosis (ALS or Lou Gehrig’s Disease). Using the standard mouse model of ALS (G93A mutant form of Cu, Zn superoxide dismutase or SOD1), we have identified two classes of compounds which dramatically extend survival, even when administered at onset of disease—equivalent to the earliest time point when human therapy can begin. Based on results from our laboratory, a Phase I human clinical trial in ALS is now underway and a second, combined Phase II/III trial will begin in early 2006. We are using several approaches to elucidate the molecular mechanisms of protection by these compounds and the mechanisms of superoxide dismutase mutant-mediated pathogenesis in the ALS mice. In addition, we maintain an active interest in identifying proteins which are targets of endogenous oxidants. Identification of these target proteins is used to help understand the fundamental mechanisms of oxidative injury in a number of human disease conditions, and to aid in rational design of pharmacological agents capable of scavenging biological oxidants and thereby preventing injury. State-of-the-art equipment and techniques including 2-D gel, mass spectrometry proteomics, sophisticated molecular modeling, HPLC, atomic absorption spectroscopy, dynamic laser light scattering, ICP-MS, and real-time PCR are used in conjunction with model systems involving recombinant proteins in vitro, cell culture, and whole animals to address fundamental biological, biochemical, and pharmacological questions.

E-mail
JPCrow@uams.edu

Selected Publications
Shoemaker JL, Seely KA, Reed RL, Crow JP, Prather PL. The CB2 cannabinoid agonist AM-1241 prolongs survival in a transgenic mouse model of amyotrophic lateral sclerosis when initiated at symptom onset. J Neurochem. 2007 (in press).

J.P. Crow. Catalytic antioxidants to treat amyotrophic lateral sclerosis. Expert Opin Investig Drugs. 2006 Nov;15(11):1383-93. Review.

S. Petri, M. Kiaei, K. Kipiani, J. Chen, N. Y. Calingasan, J. P. Crow, and M. F. Beal. Additive neuroprotective effects of a histone deacetylase inhibitor and a catalytic antioxidant in a transgenic mouse model of amyotrophic lateral sclerosis. Neurobiol.Dis., 2005.

J. P. Crow, N. Y. Calingasan, J. Chen, J. L. Hill, and M. F. Beal. Manganese porphyrin given at symptom onset markedly extends survival of ALS mice. Ann. Neurol. 58 (2):258-265, 2005.

A. S. Wu, M. Kiaei, N. Aguirre, J. P. Crow, N. Y. Calingasan, S. E. Browne, and M. F. Beal. Iron porphyrin treatment extends survival in a transgenic animal model of amyotrophic lateral sclerosis. J. Neurochem. 85 (1):142-150, 2003.

R. Rakhit, J. P. Crow, J. R. Lepock, L. H. Kondejewski, N. R. Cashman, and A. Chakrabartty. Monomeric Cu,Zn-superoxide Dismutase Is a Common Misfolding Intermediate in the Oxidation Models of Sporadic and Familial Amyotrophic Lateral Sclerosis. J. Biol. Chem. 279 (15):15499-15504, 2004.

Crow JP. Peroxynitrite scavenging by metalloporphyrins and thiolates. Free Radical Biology and Medicine 28:1487-1494, 2000.

Estévez AG, Crow JP, Sampson JB, Reiter C, Zhuang Y, Richardson GJ, Tarpey MM, Barbeito L, Beckman JS. Zinc-deficient superoxide dismutase induces motor neuron apoptosis via a nitric oxide-dependent mechanism. Science 286: 2498-2500, 1999. Crow and Estevez contributed equally to this work.

View Dr. Crow's complete PubMed publication listing.

University of Arkansas for Medical Sciences
Department of Pharmacology and Toxicology
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