Vitamin B12 is necessary for the myelin sheath covering the axon of the neuron, and for the production of the amino acid homocysteine, which has recently been linked to Alzheimer's disease when vitamin B12 levels are low. It has been reported that vitamin B12 deficiency is found in 40% of the population. The deficiency is common in the elderly population because of a common condition called Atrophic Gastritis type B, which affects the stomach mucous membrane and leads to vitamin B12 malabsorption. With an elderly population at risk for a Vitamin B12 deficiency, it is necessary to understand the effect of Vitamin B12 in Ineurodegeneration.

In the study I performed, mutant C.elegans with fluorescent dopamine neurons were exposed to three concentrations of Bisphenol-A in order to find the concentration of BPA that would cause degeneration but not mortality. Once the BPA concentration was found to cause degeneration, C.elegans were supplemented with two different types of synthetic vitamin B12, cyanocobalamin, and methylcobalamin, at two different concentrations. Cyanocobalamin is the most common type of vitamin B12 that is found in most supplements and fortified food, and methylcobalamin is more expensive but thought to be better retained in the human body. One concentration of vitamin B12 represents the recommended daily value for humans, which was made proportional to the mass of a C.elegans, and two times the recommended daily value.

I hypothesized that all both forms and concentrations of vitamin B12 would prevent neurodegeneration.

To quantify the data, fluorescent microscopy was used to take pictures of the dopamine neurons. To measure the fluorescence, I analyzed the pictures using ImageJ software. I compared the fluorescence of the background of the image to the fluorescence of the neuron. A series of calculations were done to account for the variations in the area of the neuron, the integrated density, and the difference of fluorescence between the neuron and the background. This process produced the CTAF value, which was then averaged per exposure type.

Through the ANOVA statistical analysis test, the fluorescence between the C.elegans neurons exposed to BPA was significantly lower from the control neurons, which suggests that BPA did cause neurodegeneration. Then, ANOVA determined that the neurons exposed to BPA and supplemented with all concentrations of vitamin B12 had a significantly higher fluorescence than neurons exposed to BPA. ANOVA also determined that there was no statistical significance among the neurons exposed to the types and concentrations of vitamin B12. The data analysis of the efficacy of all forms and concentrations of vitamin B12 suggests that vitamin B12 did prevent the dopamine neuron degeneration. My study suggests that supplementing with vitamin B12 is an effective method of preventing dopamine neuron degeneration in C.elegans.