Dr. Sarah Raissi, UCSF, San Francisco, California
Assessing the molecular pathways involved in myelination and normal function in Schwann cells
Dr. Raissi is exploring how CMT causes motor or sensory dysfunction through damage to peripheral neurons or myelin, the supportive coating that speeds nerve signaling. She is focusing on multiple forms of CMT in which myelin is damaged due to mutations in genes involved in the phosphoinositide signaling pathway, which is critical for proper myelin formation and maintenance. Dr. Raissi will test the hypothesis that loss of SMIT1 impairs phosphoinositide signaling in Schwann cells, leading to CMT-like myelin deficits, and that restoring this signaling can rescue these deficits. This project will investigate how the SMIT1 signaling pathway operates during normal formation and maintenance of myelin to better understand how these processes may be compromised in CMT diseases.
I am excited to partner with CMTRF to study basic mechanisms governing Schwann cell maturation and myelination of peripheral nerves. I will investigate a critical signaling pathway impaired across multiple forms of CMT, which I hope will inform our understanding of these CMT subtypes and potentially provide alternative therapeutic targets for their treatment.
