Iron Metabolism in Ts65Dn mice, a Model of Down syndrome

Iron homeostatic dysregulation may occur among individuals with Down syndrome (Ds) over their lifetime resulting in tissue iron accumulation and oxidative stress, which may be contributing factors in the development of Ds clinical outcomes. While the Ts65Dn mouse is the most extensively studied murine model of Ds that displays a remarkable number of Ds phenotypes, insight into mechanisms of iron homoeostatic regulation in the Ts65Dn model is distinctly lacking. This work is relevant to public health in its aims to establish the iron homeostatic phenotype of Ts65Dn mice and to explore the efficacy of the model to study iron as a potential mechanism of Ds-related pathologies.