Donald W. Reynolds Institute on Aging
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Donald W. Reynolds Institute on Aging

Research Faculty - Steven Barger, Ph.D.

Steven Barger, Ph.D.

Steven Barger, Ph.D. is an Associate Professor of Geriatrics and Neurobiology & Developmental Sciences at UAMS. The primary focus of Dr. Barger’s laboratory is the pathogenesis of Alzheimer’s disease. A major topic is the suspected role of inflammation in the events related to development and progression of this disease. The laboratory has explored the behavior of microglia, the resident monocytic phagocytes of the central nervous system. Dr. Barger has documented novel proinflammatory actions of the peptide derivatives of the amyloid precursor protein, including the elevation of neurotransmitters that can damage or kill neurons through hyperstimulation (“excitotoxicity”). He also maintains an interest in the potential protection against such damage provided by proteins and neurotransmitters through effects on gene expression. Specifically, a transcriptional control system has been identified that is modulated by neuroprotective agents and neurotoxins. This system involves competitive and cooperative interactions between the Rel and Sp1 families of transcription factors, with evidence for functional nuances specific to cerebral neurons.

Selected Publications:

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

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

Neuroinflammation Working Group (S.W. Barger, P. Eikelenboom, C.E. Finch, P.L. McGeer, J. Rogers, et al.). Inflammation and Alzheimer’s disease. Neurobiol. Aging, 2000. 21:383-421.

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

Mao, X., Moerman, Andrea, and Barger, S.W. Neuronal kappa-B-binding factors consist of Sp1-related proteins: Functional implications for autoregulation of NR1 expression. J Biol Chem, 2002. 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 α-peptide. J. Neuroinflammation 1:2-12.



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Donald W. Reynolds Institute on Aging

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