Steve W. Barger, Ph.D.

Steve W. Barger, Ph.D.Title
Professor of Geriatrics, Neurobiology and Developmental Sciences, and Internal Medicine

PhD
Vanderbilt University, 1992 (Cell Biology)

Major Interests
Areas of Interest: Dr. Barger’s primary interest is in the events related to neuronal death caused by pathological insults (especially, excitotoxicity) and the protection against these insults afforded by changes in gene expression. Particular focus has been given to interactions between proteins implicated in the pathogenesis of Alzheimer’s disease. His laboratory also characterizes effects of these proteins and neurotransmitters on gene expression. A transcription factor has been identified that is activated by neuroprotective agents and suppressed by neurotoxins. This factor binds promoter elements present in the genes for antioxidant enzymes and an inhibitor of apoptotic cell death. Dr. Barger and coworkers have also documented a production of excitotoxic neurotransmitters by microglia, a specialized immune cell that resides in the central nervous system. When activated by agents associated with Alzheimer’s disease, microglia produce and release harmful amounts of two such excitotoxins. Current work seeks to characterize the mechanisms involved in these effects.

Email: sbarger@uams.edu

Phone: 501-526-5811

Selected Publications

Barger, S.W., and Harmon, A.D. 1997. Microglial activation by Alzheimer amyloid precursor protein and modulation by apolipoprotein E. Nature 388: 878-881.

Hutchins, J.B., and Barger, S.W. 1998. Why neurons die: cell death in the nervous system. Anatomical Record, The New Anatomist 253: 79-90.

Mao, X., Moerman, A.M., Lucas, M.M., and Barger, S.W. 1999. Inhibition of the activity of a neuronal kB-binding factor by glutamate. J. Neurochem. 73: 1851-1858.

Mattson, M.P., and Barger, S.W. 2000. Silencing survival data. Trends Neurosci. 23: 466-467.

Barger, S.W., Basile, A.S. 2001. Activation of microglia by secreted amyloid precursor protein evokes glutamate release by cystine exchange and attenuates synaptic function. J. Neurochem. 76: 846-854.

Mao, X., Moerman, A.M., Barger, S.W. 2002. Neuronal kappaB-binding factors consist of Sp1-related proteins: Functional implications for autoregulation of NR1 expression. J. Biol. Chem. 277: 44911-44919.

Wu, S-Z., Bodles, A.M., Porter, M.M., Griffin, W.S.T., Basile, A.S., Barger, S.W. 2004. Induction of serine racemase expression and D-serine release from microglia by amyloid â-peptide. J. Neuroinflammation 1: 2-12.

Bodles, A.M., Barger, S.W. 2004. Cytokines and the aging brain – what we don’t know might help us. Trends Neurosci. 27: 621-626.

Mao, X., Moerman-Herzog, A.M., Wang, W., Barger, S.W. 2006. Differential transcriptional control of the superoxide dismutase-2 kappaB element in neurons and astrocytes. J. Biol. Chem. 281: 35863-35872

Mao, X., Yang, S.-H., Simpkins, J.W., Barger, S.W. 2007. Glutamate receptor activation evokes calpain-mediated degradation of Sp3 and Sp4, the prominent Sp-family transcription factors in neurons. J. Neurochem. 100: 1300-1314.

Barger, S.W., Goodwin, M.E., Porter, M.M., Beggs, M.L. 2007. Glutamate release from activated microglia requires the oxidative burst and lipid peroxidation. J. Neurochem. 101:1205-1213.