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| First Name: | Steve | | Last Name: | Barger | | Title: | Professor of Geriatrics, Neurobiology & Developmental Sciences | | Advanced Degrees: | Ph.D. | | Affiliation: | University of Arkansas for Medical Sciences | | Department: | Geriatrics, Anatomy & Neurobiology | | Street Address 1: | 629 Jack Stephens Dr. | | Street Address 2: | Slot 807 | | City: | Little Rock | | State/Province: | AR | | Zip/Postal Code: | 72205 | Country/Territory: | U.S.A. | | Phone: | 501-526-5811 | | Fax: | 501-526-5830 | | Email Address: |  |
Disclosure:
(view policy)
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Member reports the following financial or other potential conflicts of interest: [Last Modified: 4 September 2012]
My employer requires that I disclose that I receive royalties from Sigma-Aldrich related to the sales of secreted amyloid precursor protein (sAPP) products.
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View all comments by Steve Barger
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Alzheimer Disease, Aging Process
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Animal Models, Protein structure/chemistry, A-beta PP/A-beta, Neurobiology, Chemistry/Pharmacology, Oxidative Stress, Apoptosis/Cell cycle, DNA microarrays, Genetics, Microscopy, Molecular and Cell biology, Neuropathology, Signal transduction, Neuroimmunology, Neurotransmission
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University, Research institute
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Dr. Barger graduated from Hendrix College in 1987 with the Spessard Biology Award, then entered the Department of Cell Biology graduate program at Vanderbilt University. After receiving his Ph.D. in 1992, Dr. Barger began a postdoctoral fellowship at the Sanders-Brown Center on Aging at the University of Kentucky, where he received an award from the French Foundation for Alzheimer's Research and an National Institutes of Health (NIH) National Research Service Award. In 1995, he returned to his home state of Arkansas to become the first recipient of the Inglewood Fellowship for Alzheimer's research, as well as an Assistant Professor of Internal Medicine and Anatomy at the University of Arkansas for Medical Sciences. Dr. Barger received the annual research award from the Neurosciences Education and Research Foundation in 1999. He currently holds two NIH-sponsored grants, advises a graduate student and four postdoctoral fellows. He is an editor for Journal of Neurochemistry, Journal of Neuroinflammation, Journal of Neuroscience Research, Neurobiology of Aging, and Current Alzheimer Research. He has served as President of the Arkansas Chapter of the Society and on the SfN Committee for Animals in Research. Dr. Barger is also a member of the Arkansas Center for Neuroscience and the International Society for Neurochemistry. |
Barger, S.W., and Harmon, A.D. 1997. Microglial activation by Alzheimer amyloid precursor protein and modulation by apolipoprotein E. Nature 388: 878-881.
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.
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 β-peptide. J. Neuroinflammation 1:2-12.
Mao, X., Moerman-Herzog, A.M., Wang, W., Barger, S.W. 2006. Neuronal Sp-factors act as transcriptional repressors via a κB-element in the SOD2 gene. 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. (in press)
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Everything! It still seems quite obscure. |
Studies of neurodegeneration in long-lived species, particularly primates. |
Neuroinflammation in AD (and other conditions) involves the release of excitotoxic amino acids from microglia. |
Several experiments with safe and effective glutamate receptor antagonists could be supportive. |
Amyloid beta-peptide accumulates and exerts a direct and detrimental effect on synaptic function. |
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