Erin M. Gibson

Erin M. Gibson is a glial and circadian biologist as well as an assistant professor in the Department of Psychiatry and Behavioral Sciences and the Stanford Center for Sleep Sciences and Medicine at Stanford University. Gibson investigates the role of glial cells in sculpting neural circuits and mechanistically probes how the circadian rhythm modulates glial biology.

Early life and education Gibson grew up in St. Louis, Missouri, and attended Whitfield School for her secondary education. Gibson became interested in neuroscience after participating in a research internship at Washington University in St. Louis, an opportunity encouraged by her biology teacher. As an undergraduate researcher, Gibson worked under Christina Williams in the Department of Psychology and Neuroscience. In Williams' lab, Gibson explored how nutrients and hormones alter brain development and behavior. Gibson graduated from Duke in 2005 with a Bachelors of Science degree. Her undergraduate work also helped elucidate that prenatal choline supplementation alleviates age-related declines in exploratory behavior in rats.

In 2006, Gibson moved to the West Coast to pursue her graduate studies at the University of California, Berkeley, She discovered a novel mammalian RFamide-related peptide (RFRP) that acted upstream of gonadotropin-releasing hormone (GnRH) to inhibit its release and prevent an LH surge throughout most of the reproductive cycle. To explore how circadian disruptions affect the brain, Gibson used a technique called experimental jet lag where she introduced phase advances in the light:dark cycle of female hamsters, similar to phase shifts one might experience when traveling to a new time zone. Her findings on the effects of circadian disruption on learning and memory highlight the implications of international travel on cognitive function. Her work was highlighted in ABC Science, The Wall Street Journal, NPR and Time. Gibson's thesis, titled "The Role of the Circadian System in Reproductive, Neural, and Immune Health" summarized her experimental findings during her graduate work to emphasize the importance of circadian biology in health and disease. Gibson sought to understand how chemotherapy alter the brain by focusing her attention on glial cells, particularly myelin-making glial cells called oligodendrocytes since demyelinating disorder is associated with chemotherapy-related cognitive impairment. Her results highlight a potential avenue with which to treat demyelinating diseases through the modulation of neural activity. After developing a mouse model of methotrexate chemotherapy-induced neurological dysfunction, Gibson and her colleagues found decreases in oligodendrocyte precursor cells (OPCs). Gibson's lab explores the cellular and molecular mechanisms that modulate glial cells in the central nervous system. The group came together to address the childcare-conference conundrum in which women are less able to attend conference due to the lack of childcare available at these events. In 2020, Gibson also wrote a piece in Science addressing the importance of welcoming personal disclosures when institutions and review committees evaluate scientists' curricula vitae. Personal disclosures will help to address the unforeseen life events that might impact ones' research and career trajectory but are often left unaccounted for, only noted as gaps in a scientists' curriculum vitae.

Select publications

Gibson EM, Nagaraja S, Ocampo A, Tam L, Wood LS, Pallegar PN, Greene JJ, Geraghty AC, Goldstein AK, Ni L, Woo PJ, Barres BA, Liddelow SA, Vogel H, & Monje M (2019). Methotrexate chemotherapy induces persistent tri-glial dysregulation that underlies chemotherapy-related cognitive impairment. Cell, 176, 43–55. Gibson EM & Monje M. Emerging mechanistic underpinnings and therapeutic targets for chemotherapy-related cognitive impairment (2019). Current Opinion in Oncology. Geraghty AC, Gibson EM, Ghanem RA, Greene JJ, Ocampo A, Goldstein AK, Ni L, Yang T, Marton RM, Pasca SP, Greenberg ME, Longo FM, & Monje M (2019). Loss of adaptive myelination contributes to methotrexate chemotherapy-related cognitive impairment Neuron, 103, 2, 250–265. Gibson EM, Geraghty AC, & Monje M (2017). Bad Wrap: Myelin and Myelin Plasticity in Health and Disease. Developmental Neurobiology, 78, 2, 123–135. Purger D, Gibson EM, & Monje M (2016). Myelin plasticity in the central nervous system. Neuropharmacology, 110(Pt B), 563–573. Venkatesh HS, Johung TB, Caretti V, Noll A, Tang Y, Nagaraja S, Gibson EM, Mount CW, Polepalli J, Mitra SS, Woo PJ, Malenka RC, Vogel H, Bredel M, Mallick P, & Monje M (2015). Neuronal activity-regulated secretion of neuroligin-3 promotes glioma growth. Cell, 161, 803–816. Gibson EM, Purger D, Mount CW, Goldstein AK, Lin GL, Wood LS, Inema I, Miller SE, Bieri G, Zuchero JB, Barres BA, Woo PJ, Vogel H, & Monje M (2014). Neuronal activity promotes oligodendrogenesis and adaptive myelination in the mammalian brain. Science, 2014; 344 (6183): 487-? Gibson E & Monje M (2012). Effect of cancer therapy on neural stem cells: implications for cognitive function. Current Opinion in Oncology, 24,6. Gibson EM, Wang C, Tjho S, Khattar N & Kriegsfeld LJ (2010). Experimental 'jet lag' inhibits adult neurogenesis and produces long-term cognitive deficits in female hamsters. PLOS One, 5,12. Gibson EM, Williams WP, & Kriegsfeld LJ (2009). Aging in the circadian system: Considerations for health, disease prevention, and longevity. Experimental Gerontology, 44, 1–2, 51–56. Gibson EM, Humber SA, Jain S, Williams WP, Zhao S, Bentley GE, Tsutsui K, & Kriegsfeld LJ (2008). Alterations in RFamide-related peptide expression are coordinated with the preovulatory luteinizing hormone surge. Endocrinology, 149, 10, 4958–4969.