DescriptionMyelination of axons increases the efficiency of the nervous system by increasing the conductivity of the action potentials. Peripheral demyelinating diseases are prevalent disorders caused by impairments in Schwann cell myelination with no currently available cure. The objective of this thesis is to describe the role of choline metabolism in peripheral nervous system myelination. The myelin sheath is comprised of a large percentage of phospholipids and choline is the major precursor to many of its lipid components. The choline-phosphatidylcholine pathway generates phosphoinositide which important in lipid biosynthesis as well as intracellular signaling and endomembrane trafficking. The imbalance of phosphoinositide levels, particularly PI(3,5)P2, has been implicated in abnormal myelin formation. In fact, pathways regulating phosphoinositide levels are impaired in multiple peripheral demyelinating diseases underscoring the importance of understanding the role of choline metabolism in Schwann cell myelination. Choline also has regulatory effects on DNA and histone methylations, making it an important component for epigenetic modifications in Schwann cells. By gaining a better understanding of the molecular mechanisms that contribute to demyelinating disorders, specifically related to choline metabolism, we can develop effective therapeutic treatments.