Effects of Vitamin B12 Supplementation on Neurodegeneration in an Alzheimer’s Disease Model of Drosophila melanogaster
Faculty Mentor
Theodore Brummel
Area of Research
Biology
Major
Biology, Pre-Medical Sciences
Description
INTRODUCTION: This study investigates the effects of vitamin B12 supplementation on neurodegeneration associated with Alzheimer’s disease using Drosophila melanogaster as a model organism. It was hypothesized that vitamin B12 would attenuate neurodegenerative progression, while the null hypothesis stated that vitamin B12 would have no significant effect.
METHOD: To generate the Alzheimer's model a conditional expression system was used (GAL4 UAS) to express the pathogenic version of the amyloid beta precursor protein 42 throughout the nervous system. This is a validated strategy for modeling Alzheimer’s disease. Wild type and Alzheimer’s flies were maintained at 29º C on either standard yeast sucrose media or yeast sucrose media supplemented with vitamin B12. Neurodegeneration was quantified using negative geotaxis assays to assess locomotor function, as well as lifespan analysis to evaluate overall survival.
RESULTS: Data from these assays were collected and analyzed to determine the impact of vitamin B12 on disease progression. Results are currently being analyzed to assess whether vitamin B12 supplementation provides a protective effect against neurodegeneration.
DISCUSSION/CONCLUSION: It was hypothesized that vitamin B12 would attenuate neurodegenerative progression.
Effects of Vitamin B12 Supplementation on Neurodegeneration in an Alzheimer’s Disease Model of Drosophila melanogaster
INTRODUCTION: This study investigates the effects of vitamin B12 supplementation on neurodegeneration associated with Alzheimer’s disease using Drosophila melanogaster as a model organism. It was hypothesized that vitamin B12 would attenuate neurodegenerative progression, while the null hypothesis stated that vitamin B12 would have no significant effect.
METHOD: To generate the Alzheimer's model a conditional expression system was used (GAL4 UAS) to express the pathogenic version of the amyloid beta precursor protein 42 throughout the nervous system. This is a validated strategy for modeling Alzheimer’s disease. Wild type and Alzheimer’s flies were maintained at 29º C on either standard yeast sucrose media or yeast sucrose media supplemented with vitamin B12. Neurodegeneration was quantified using negative geotaxis assays to assess locomotor function, as well as lifespan analysis to evaluate overall survival.
RESULTS: Data from these assays were collected and analyzed to determine the impact of vitamin B12 on disease progression. Results are currently being analyzed to assess whether vitamin B12 supplementation provides a protective effect against neurodegeneration.
DISCUSSION/CONCLUSION: It was hypothesized that vitamin B12 would attenuate neurodegenerative progression.