Publication Date

2017

Document Type

Thesis

Committee Members

Nancy Bigley (Advisor), Barbara Hull (Committee Member), Shulin Ju (Committee Member)

Degree Name

Master of Science (MS)

Abstract

This study examined the inflammatory effects of amyloid-ß (Aß42) 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 Aß42. This culture system, when seeded with Aß42, serves as an in vitro model for Alzheimer’s disease (AD). In a neuronal-microglia co-culture, Aß42 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.

Page Count

63

Department or Program

Microbiology and Immunology

Year Degree Awarded

2017


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