The goal of my research is to identify therapies for Alzheimer's disease (AD). I have hypothesized that enhancing one carbon metabolism with the methyl donor betaine will improve mitochondria in a mouse model of AD by decreasing the levels or activity of DRP₋₁. This protein causes excess fission of mitochondria in AD which generates smaller mitochondria that are unable to make enough energy. I am testing my hypothesis by administering betaine (1%) in drinking water to 1-month and 3-month (n=3) AD mice and measuring the effects on DRP₋₁ and mitochondrial size.