Does a 2x dose of different Vitamin B12 forms affect Tau phosphorylation and expression of proteins that regulate Tau phosphorylation?
Document Type
Event
Abstract
Vitamin B12 consumption has been increasing since the mid-1990s after the fortification of grains with folic acid and Vitamin B12. As consumption of Vitamin B12 has increased, prevalence of Autism Spectrum Disorders (ASD) has also increased. In 2020, 1 in 54 children in the U.S. was diagnosed with ASD. Individuals with ASD commonly possess a mutation in methyltetrahydrofolate reductase enzyme (MTHFR). This mutation leads to a loss of folic acid metabolism to a one-carbon methyl group in the cell. ASD is now known to have both genetic and epigenetic components. Loss of MTHFR function seen in ASD patients likely changes Vitamin B12 usage and affects epigenetics. Therefore, excess Vitamin B12 may affect gene expression. As a result, we investigated the effects of 3 Vitamin B12 forms: +2 Cobalt cyanocobalamin, +3 Cobalt cyanocobalamin, and cobamamide at a 2x dose, with and without a knockdown of MTHFR expression, on gene expression of several kinases involved in phosphorylation and dephosphorylation of Tau. Using a neurobiological model, the SHSY5Y cell, we hypothesized increased Tau phosphorylation for the +3 Cobalt cyanocobalamin and Cobamamide forms and hypothesized that the +2 Cobalt cyanocobalamin would have no effect on Tau phosphorylation, based on previous findings in the lab.
Does a 2x dose of different Vitamin B12 forms affect Tau phosphorylation and expression of proteins that regulate Tau phosphorylation?
Breakout Session B: Biological Sciences
CLC BallroomVitamin B12 consumption has been increasing since the mid-1990s after the fortification of grains with folic acid and Vitamin B12. As consumption of Vitamin B12 has increased, prevalence of Autism Spectrum Disorders (ASD) has also increased. In 2020, 1 in 54 children in the U.S. was diagnosed with ASD. Individuals with ASD commonly possess a mutation in methyltetrahydrofolate reductase enzyme (MTHFR). This mutation leads to a loss of folic acid metabolism to a one-carbon methyl group in the cell. ASD is now known to have both genetic and epigenetic components. Loss of MTHFR function seen in ASD patients likely changes Vitamin B12 usage and affects epigenetics. Therefore, excess Vitamin B12 may affect gene expression. As a result, we investigated the effects of 3 Vitamin B12 forms: +2 Cobalt cyanocobalamin, +3 Cobalt cyanocobalamin, and cobamamide at a 2x dose, with and without a knockdown of MTHFR expression, on gene expression of several kinases involved in phosphorylation and dephosphorylation of Tau. Using a neurobiological model, the SHSY5Y cell, we hypothesized increased Tau phosphorylation for the +3 Cobalt cyanocobalamin and Cobamamide forms and hypothesized that the +2 Cobalt cyanocobalamin would have no effect on Tau phosphorylation, based on previous findings in the lab.