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laura.fonken@austin.utexas.edu
Phone: 512-232-8331
Office Location
BME 3.510C
Postal Address
107 W DEAN KEETON ST
AUSTIN, TX 78712-
Assistant Professor in the Department of Pharmacology and Toxicology at the University of Texas at Austin
Dr. Fonken completed her PhD in Neuroscience in Dr. Randy Nelson’s laboratory at The Ohio State University. Laura’s dissertation research focused on the effects of nighttime light exposure on physiology and behavior. Next, Laura completed a post-doctoral fellowship in Dr. Steven Maier’s laboratory in the Department of Psychology and Neuroscience at the University of Colorado Boulder. In the Maier laboratory, Laura’s research focused on understanding how heightened neuroinflammatory responses contribute to mood disorders and cognitive impairments with aging. Current research in her laboratory focuses on endogenous (e.g. circadian rhythms) and exogenous (e.g. infection and injury) factors that influence neuroimmune function across the lifespan.
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Research in the Fonken lab broadly focuses on how interactions between the immune, nervous, and endocrine systems can regulate complex behavioral processes such as cognitive and mood related behaviors. Resident immune cells, called microglia, were first identified in the brain by Del Rio-Horetga over 100 years ago. These cells were initially thought to have a passive role in the healthy brain and only become active during CNS injury. However, we now know that glial cells have a diverse array of functional roles in maintaining brain homeostasis and in responding to CNS pathology. For example, microglia are involved in synaptic development and pruning, neuronal migration, and progenitor cell differentiation. Microglia form and function are tightly regulated in the CNS to help regain homeostasis following activation. However, the neuroimmune system is sensitive to a number of environmental challenges and dysregulation of neuroimmune function is implicated in neuropsychiatric disorders including depression, schizophrenia, and cognitive dysfunction. Thus, our current research focuses on understanding how endogenous (e.g. circadian rhythms and aging) and exogenous (e.g. environmental pollutants, infection, and injury) factors that influence neuroimmune function drive cognitive and affective behavioral changes.
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1. Fonken, L.K., Frank, M.G., D’Angelo, H.M., Heinze, J.D., Watkins, L.R., Lowry, C.A., & Maier, S.F. (2018). Mycobacterium vaccaeimmunization protects aged rats from surgery-elicited neuroinflammation and cognitive dysfunction. Neurobiology of Aging: In press.
2. Frank, M.G., Fonken, L.K., Watkins, L.R., Maier, S.F., & Lowry, C.A. (2018). Could probiotics be used to mitigate neuroinflammation? ACS Chemical Neuroscience: In press.
3. Fonken, L.K., Frank, M.G., Gaudet, A.D., & Maier, S.F. (2018). Stress and aging act through common mechanisms to elicit neuroinflammatory priming. Brain, Behavior, and Immunity: In press.
4. Frank, M.G., Fonken, L.K., Dolzani, S.D., Annis, J.L., Siebler, P.H., Heinze, J.D., Schmidt, D., Watkins, L.R., Maier, S.F., & Lowry, C.A. (2018). M. vaccae treatment induces an anti-inflammatory milieu in the CNS: attenuation of stress-induced microglial priming, alarmins, and anxiety-like behavior. Brain, Behavior, and Immunity: In press.
5. Gaudet, A.D. & Fonken, L.K. (2018). Glial cells shape pathology and repair after spinal cord injury. Neurotherapeutics: In press.
6. Sun, Q., Zhang, G., Chen, R., Wang, H., Jiang, A., Li, Z., Li, R., Kong, K., Fonken, L.K., Rajagopalan, S., Sun, Q., & Lui, C. (2018). Central IKK2 inhibition ameliorates air pollution mediated hepatic glucose and lipid metabolism dysfunction in mice with type II diabetes. Toxicological Sciences: 164 (1): 240-249.
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