Degree Name
MS (Master of Science)
Program
Biology
Date of Award
5-2018
Committee Chair or Co-Chairs
Patrick Bradshaw
Committee Members
Yue Zou, Wright Gary, Michelle Chandley
Abstract
Alzheimer’s disease (AD) is associated with amyloid-beta peptide deposition and loss of mitochondrial function. Using a transgenic C. elegans AD worm model expressing amyloid-beta in body wall muscle, we determined that supplementation with either of the forms of vitamin B2, flavin mononucleotide (FMN) or flavin adenine dinucleotide (FAD) protected against amyloid-beta mediated paralysis. FMN and FAD were then assayed to determine effects on ATP, oxygen consumption, and reactive oxygen species (ROS) with these compounds not significantly improving any of these mitochondrial bioenergetic functions. Knockdown of the daf-16/FOXO transcriptional regulator or the FAD synthase enzyme completely abrogated the protective effects of FMN and FAD, while knockdown of the mitochondrial unfolded protein response factors ubl-5 or atfs-1 also blocked the protective effects. Therefore, vitamin B2 supplementation could lead to the activation of conserved signaling pathways in humans to delay the onset and progression of neurodegenerative diseases such as AD.
Document Type
Thesis - unrestricted
Recommended Citation
Ameen, Muhammad Tukur, "A Role of Vitamin B2 in Reducing Amyloid-beta Toxicity in a Caenorhabditis elegans Alzheimer’s Disease Model" (2018). Electronic Theses and Dissertations. Paper 3398. https://dc.etsu.edu/etd/3398
Copyright
All Rights Reserved
Included in
Biology Commons, Molecular and Cellular Neuroscience Commons, Molecular Biology Commons, Nervous System Diseases Commons