Patrick C. Duncker received his B.S. in Biology, with a minor in Psychology, at the University of California, Irvine in 2009. He joined the Graduate Program in Immunology at the University of Michigan in 2012. In 2013, he joined the laboratory of Dr. Benjamin Segal, and is on track to complete to complete his graduate training in the winter of 2018.
During his undergraduate studies, Patrick’s scientific interests were focused on neuronal damage, protection, and regeneration. In an animal model of Parkinson’s disease, he studied the migration and differentiation of ependymal cells toward exogenous transforming growth factor alpha infused into the striatum. The study sought to show the potential of these cells to function as endogenous adult neural stem cells in the brain. Further, induced migration and differentiation of these cells may provide benefits for diseases marked by neural damage, such as Parkinson’s Disease, Multiple Sclerosis, and Alzheimer’s Disease.
His undergraduate research project aimed to provide neuroprotection again large dose administration of methamphetamine. Binge administration of methamphetamine leads to extensive production of dopamine , glutamate, and serotonin leading to irreversible loss of nerve terminals throughout the striatum and cerebral cortex of the brain. Epidural administration of glutamate receptor antagonists, or administration of dopamine receptor antagonists into the striatum, lead to widespread sparing of dopamine , glutamate, and serotonin synapses throughout the brain.
Upon completion of his undergraduate degree, Patrick worked as a laboratory technician for Dr. Thomas Lane at UC Irvine. Here he was introduced to the interplay of immunology and neuroscience. The projects in which he was engaged utilized a viral-induced model of central nervous system (CNS) demyelination, and sought to understand the immunological mechanisms involved in CNS damage and repair. Using this model, he was involved in demonstrating that Epstein-Barr virus-induced gene 3 negatively regulates viral neuroinflammation by modulating the proinflammatory T cell response to the virus.
2016 – Finalist for Best Poster Presentation, Americas Committee for Treatment and Research in Multiple Sclerosis (ACTRIMS)
2018 – Second Place, Best Young Investigator Oral Presentation, ACTRIMS
Duncker PC, Segal BM (2018, July). GM-CSF Induces CCR1 Ligand Production by CNS-Infiltrating Myeloid Cells, Driving Chronic Disability During EAE. Oral presentation and poster presented at Federation of American Societies for Experimental Biology: Translational Neuroimmunology. Snowmass, CO.
Duncker PC, Segal BM (2018, February). GM-CSF Induces CCR1 Ligand Production by CNS-Infiltrating Myeloid Cells, Driving Chronic Disability During EAE. Oral presentation and poster presented at ACTRIMS Forum 2018, San Diego, CA. DOI: 10.1177/1352458518761737.
Duncker PC, Stoolman JS, Huber AK, Segal BM (2017, February). Granulocyte-Macrophage Colony-Stimulating Factor Drives Chronic Disability In Autoimmune Demyelinating Disease. Poster presented at ACTRIMS Forum 2017, Orlando, FL. DOI: 10.1177/1352458517693959 #P096.
Duncker PC, Stoolman JS, Huber AK, Segal BM (2016, February). Granulocyte-Macrophage Colony-Stimulating Factor: Pleiotropic Roles in Autoimmune Encephalomyelitis. Poster presented at ACTRIMS Forum 2016, New Orleans, LA. Abstract.
Duncker PC, Stoolman JS, Huber AK, Segal BM (2015, October). Granulocyte-Macrophage Colony-Stimulating Factor: Pleiotropic Roles in Autoimmune Encephalomyelitis. Poster presented at the Taubman Institute Eighth Annual Symposium, Ann Arbor, MI.