Master of Science (MS)
First Committee Member
Bryan L. Spangelo
Number of Pages
A paucity of gamma-aminobutyric acid (GABA) levels is thought to encourage cytokine release in Alzheimer's disease (AD). A mechanistic investigation into the GABA-mediated suppression of the synergistic release of interleukin (IL)-6 by IL-1beta and tumor necrosis factor (TNF)-alpha is presented. Preliminary results indicate that p38 and nuclear factor (NF)-kappaB are essential for the synergistic release of IL-6 by IL-1beta and TNF-alpha. Both IL-1beta and TNF-alpha are able to stimulate the phosphorylation of p38, however, no synergistic stimulation was observed. IL-1beta or TNF-alpha is able to stimulate the degradation of the NF-kappaB inhibitor, IkappaB-alpha, with no change in IkappaB-beta. Interestingly, TNF-alpha is able to accelerate IkappaB-alpha degradation in the presence of IL-1beta. While GABA is unable to suppress IkappaB-alpha degradation and the phosphorylation of p38 by IL-1beta and TNF-alpha, it is postulated that GABA may be able to inhibit IL-6 concentrations by lessening the rate of IkappaB-alpha degradation.
Acid; Aminobutyric; Astrocytic; Cytokine; Gamma; Induction; Inhibits; Interleukin; Mechanistic; Mediated; Release; Study; Synergistic
Biochemistry; Pharmacology; Neurosciences; Cellular biology
University of Nevada, Las Vegas
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Aguinaldo, Grant Toshio, "gamma-Aminobutyric acid inhibits cytokine-mediated synergistic induction of astrocytic interleukin-6 release: A mechanistic study" (2006). UNLV Retrospective Theses & Dissertations. 2012.