Nancy Bigley (Advisor), Barbara Hull (Committee Member), Shulin Ju (Committee Member)
Master of Science (MS)
This study examined the inflammatory effects of amyloid-beta (A[beta]42) in a microglial-neuronal co-culture system and determined whether 1a, 25-dihydroxyvitamin D3 (1,25-(OH)2D3) along with suppressor of cytokine signaling (SOCS)1 and SOCS 3 mimetics would attenuate the inflammatory response to A[beta]42. This culture system, when seeded with A[beta]42, serves as an in vitro model for Alzheimer's disease (AD). In a neuronal-microglia co-culture, A[beta]42 stimulated microglia to secrete TNF-a, but with the addition of 1,25-(OH)2D3, TNF-a levels dropped by nearly eight-fold and to near zero values in the presence of both 1,25-(OH)2D3 and SOCS1 and SOCS 3 mimetics. The reduction of the inflammatory cytokine TNF-a by both 1,25-(OH)2D3 and SOCS mimetics, suggests that these molecules may be an effective means of treating AD related inflammation, and that 1,25-(OH)2D3 along with SOCS proteins mimetics should be considered for early onset AD.
Department or Program
Microbiology and Immunology
Year Degree Awarded
Copyright 2017, all rights reserved. My ETD will be available under the "Fair Use" terms of copyright law.