- Adjunct Assistant Professor of Pharmaceutical Sciences
Denise Inman, Ph.D., has investigated the mechanisms of primary open angle glaucoma development and progression for more than a decade. Her motivation has always been making a difference in our understanding of injury and disease, beginning with her graduate work in spinal cord injury at the University of Virginia. After a post-doctoral fellowship at the University of California, San Francisco in neural development, Dr. Inman moved to the University of Washington where she began her research into the role of glia in neurodegenerative disorders, with special emphasis on glaucoma. Dr. Inman has been at NEOMED since 2012.
AREA OF EXPERTISE/RESEARCH INTERESTS
Resesarch in the Inman Lab focuses on energy management and utilization through neural-glial interaction in neurodegenerative disease, with an emphasis on glaucoma. We are interested in understanding the mechanism of energy decline in the CNS with aging and disease, exploring hypotheses related to mitochondrial damage and quality control. We also investigate disease-related changes in gangliosides, which have implications for cell signaling and survival.
- Ph.D. in Neuroscience from the University of Virginia
- Human Anatomy & Physiology for Pharmacy Students
- Medical Neuroscience
- Foundations in Neuroscience
- Research Writing
- Transitions to Pharmaceutical Medicine
- Cellular Molecular Neuroscience
- Junior Faculty of the Year 2017, NEOMED
- Gonfalonier for College of Graduate Studies, NEOMED Commencement 2015
- Ohio Magazine’s Excellence in Education 2013
- Metabolic Vulnerability in the Neurodegenerative Disease Glaucoma.
- Decreased Energy Capacity and Increased Autophagic Activity in Optic Nerve Axons With Defective Anterograde Transport.
- Mitochondrial morphology differences and mitophagy deficit in murine glaucomatous optic nerve.
- Differential progression of structural and functional alterations in distinct retinal ganglion cell types in a mouse model of glaucoma.
- α-Lipoic acid antioxidant treatment limits glaucoma-related retinal ganglion cell death and dysfunction.