The microtubule affinity-regulating kinase (MARK) family is a group of proteins previously observed to play a significant role in the hyperphosphorylation of the microtubule-associated protein tau, which begins the cascade of metabolic irregularities that lead to neurodegenerative disease. Given the diverse functionality of MARKs in many cellular processes, this work seeks to explore the mechanisms involved by which neurodegeneration progresses with respect to MARK activity. Specifically, we are looking at (1) MARK regulation using SARS-COV2 Orf9b binding with MARKs as a model for kinase control, and (2) the effect of MARKs on the trafficking and distribution of the glucose transporter (GLUT) family and the subsequent implications to cellular energy metabolism. By exploring these aspects we hope to understand both the upstream and the downstream aspects of the role of MARKs in disease for their possibility as molecular targets for neurodegenerative disease intervention.