

Melissa Borgen
Assistant Professor | Biomedical and Chemical Engineering and Sciences:
Contact Information
Selected Publications
Research
What are the molecular mechanisms responsible for building and maintaining a functioning nervous system? Great strides have been made in the neuroscience field to identify molecules that regulate synapse formation. Synapse formation consists of several steps including axon outgrowth, target recognition, axon termination, synaptic assembly, and the final step, synapse maintenance. In addition to concluding the formation process, synapse maintenance is critical throughout an animal’s lifetime in order to retain circuitry and allow for synaptic plasticity. Understanding the molecular mechanisms and regulation of synapse formation and, especially, synapse maintenance, is critical, as synapse destabilization is an early hallmark of several neurodegenerative diseases, including Alzheimer’s disease. The molecular and cellular mechanisms of synapse formation and maintenance are complex. Indeed, we lack a clear understanding of how the molecular mechanisms of formation and maintenance differ, even when the same molecules are at play in both scenarios.
The goal of the Borgen Lab is to use genetics, cell biology, and live-imaging to study the intracellular molecular mechanisms that influence synapse maintenance and neurodegeneration using the C. elegans model system. Identifying new molecules that are part of the complex signaling processes that regulate synapse maintenance will be critical for developing future diagnostic and therapeutic targets for neurodegenerative diseases. C. elegans is a powerful genetic model system that is well established for studying synapse formation and maintenance. Importantly, C. elegans is a student-friendly model system. It has fast generation times and a simple and completely mapped nervous system consisting of 302-neurons. Additionally, previous work, including my own, shows that pharmacological treatment can impact synapse maintenance in C. elegans. This opens up future possibilities of using C. elegans to screen potential therapeutic compounds that affect synapse maintenance.