Degree Name
MS (Master of Science)
Program
Biology
Date of Award
5-2021
Committee Chair or Co-Chairs
Patrick C Bradshaw
Committee Members
Krishna Singh, Chad Frasier, Doug Thewke
Abstract
Alzheimer’s disease (AD) is symptomized by amyloid-beta plaques in the brain and accounts for more than 65 percent of dementia cases. Vitamin B12 (cobalamin) deficiency can result in similar cognitive impairment and roughly 15% of the elderly are vitamin B12 deficient. Vitamin B12 deficiency results in the accumulation of toxic methylmalonic acid and homocysteine. Hyperhomocysteinemia is a strong risk factor for AD. To test if vitamin B12 deficiency stimulates amyloid-beta toxicity, Caenorhabditis elegans expressing amyloid-beta in muscle were fed either vitamin B12-deficient OP50-1 or vitamin B12-rich HT115(DE3) E. coli bacteria. Increased amyloid-beta toxicity was found in worms fed the 0P50-1 diet. Supplementation of the OP50-1 diet with vitamin B12 did not rescue the increased C. elegans toxicity. Knockdown of either of the only two C. elegans vitamin B12-dependent enzymes metr-1 or mmmc-1 protected against toxicity. Therefore, vitamin B12 deficiency does not stimulate Alzheimer’s amyloid-beta-mediated toxicity in C. elegans.
Document Type
Dissertation - unrestricted
Recommended Citation
Showemimo, Opeyemi F., "Vitamin B12 Deficiency Does Not Stimulate Amyloid-beta Toxicity in a Ceanorhabditis elegans Model of Alzheimer’s Disease" (2021). Electronic Theses and Dissertations. Paper 3869. https://dc.etsu.edu/etd/3869
Copyright
Copyright by the authors.
Included in
Cognitive Neuroscience Commons, Molecular and Cellular Neuroscience Commons, Nervous System Diseases Commons, Other Neuroscience and Neurobiology Commons