RESEARCH
Unraveling the Complexities of Neuroinflammation Following Neural Injury
STROKE AND OBESITY
I am interested in studying the neuroinflammatory response to stroke, which is exacerbated in obesity. Obesity is a serious chronic inflammatory disease. People who are obese are 65% more likely to have a stroke. The interaction between this peripheral inflammatory condition and the neuroinflammatory response following stroke has not been well studied. I am interested in defining the underlying mechanistic underpinnings of the increased neuroinflammatory response seen in the obese following stroke. Shedding light on this process will lead to potential therapeutic treatments for stroke in the obese.
MICROGLIAL-ASTROCYTE INTERACTIONS
We still have only a very limited understanding of how our brain's resident immune cells, glia interact with one another. Astrocytes and microglia initiate and coordinate our brain's response to all types of disease, injury, and infection, yet we know very little about the basic fundamental signaling mechanisms underlying their response. I am interested in identifying the cellular and molecular signals these cells use to communicate with each other to coordinate their interaction with neurons and other cells involved in this neuroinflammatory process. These complex processes are involved in traumatic brain injury and stroke, brain infection, and many neurodegenerative disorders like Alzheimer's Disease and Parkinson's Disease. Understanding the mechanisms of how the glial response unfolds will lead to treatment options for many neurological disorders.
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THE RESPONSE OF DEVELOPING GLIAL CELLS IN PEDIATRIC STROKE
While pediatric stroke is common, we do not have a good understanding of how the developing brain responds to injury. We all know that neurons are still dividing and making connections well into adolescence. Our brain's immune cells are also still maturing during this time and we do not know how they may contribute to the vulnerability of the brain during its critical stages of development. Understanding and treating the neuroinflammatory response to stroke in pediatric stroke may reduce the risk of neurological and neuropsychiatric disease later in adulthood.
POST-TRAUMATIC STRESS DISORDER
Both acute and chronic stress lead to multiple long-term physiological, emotional, and behavioral effects. It has been established that alterations in glial cells accompany these effects. Specifically, alterations in key areas like the prefrontal cortex, hippocampus, amygdala, and hypothalamus have been found. We are interested in examining the cellular and molecular changes that occur in these glial cells. Identifying these important factors will increase our ability to examine this disorder and it's comorbidities like traumatic brain injury.
The main goal of our research laboratory is to understand the complex pathophysiological mechanisms following neural insult and to develop treatments that limit these mechanisms to reduce injury expansion and improve functional recovery.
SELECT PUBLICATIONS
Peterson, T. C., Brahms, E., Lui, A., Buckwalter, M. S. (2020). Obesity drives delayed infarct expansion, inflammation, and distinct gene networks in a mouse stroke model. Translational Stroke Research, doi: 10.1007/s12975-020-00826-9.
Lechtenberg, K. J., Meyer, S. T., Doyle, J. B., Peterson, T. C., Buckwalter, M. S. (2019). b2-adrenergic signaling reduces microglial and monocyte proliferation and dampens the neuroinflammatory response following ischemic stroke. Journal of Neuroinflammation, 16 (1), 112-130. doi: 10.1186/s12974-019-1506-4.
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Yousef, H., Czupalla, C. J., Lee, D., Chen, M. B., Burke, A., Zandstra, J., Berber, E., Lehallier, B., Mathur, V., Nair, R. V., Bonanno, L., Yang, A. C., Peterson, T. C., Hadeiba, H., Merkel, T., Zera, K. A., Korbelin, J., Schwaninger, M., Buckwalter, M. S., Quake, S., Butcher, E. C., Wyss-Coray, T. (2019). Aged blood activates microglia and reduces adult neural precursor cell activity through brain endothelial VCAM1 in the hippocampus. Nature Medicine.
Chaney, A., Cropper, H. C., Johnson, E. M., Lechtenberg, K. J., Peterson, T. C., Buckwalter, M. S., James, M. L. (2018). 11CDPA-713 versus and 18FGE180: A preclinical comparison of TSPO-PET tracers to visualize acute and chronic neuroinflammation in a mouse model of ischemic stroke. Journal of Nuclear Medicine, 60(1), 122-128.Doi: 10.2967/jnumed.118.209155
Liddelow, S. A., Clarke, L. E., Bennett, M. L., Bennett, F. C., Munch, A. E., Guttenplan, A. E., Shirmer, L., Chung, W., Peterson, T. C., Wilton, D. K., Frouin, A., Napier, B. A., Panicker, N., Kumar, M., Dawson, V. L., Dawson, T. M., Buckwalter, M. S., Rowitch, D. H., Stevens, B., & Barres, B. A. (2017). Neurotoxic reactive astrocytes are induced by activated microglia. Nature, 00, 1-7. Doi: 10.1038/nature21029.
Vonder Haar, C.*, Peterson, T. C.*, Martens, K. M., Hoane, M. R. (2016). Vitamins and nutrients as primary treatments in experimental brain injury: Clinical implications and for nutraceutical therapies. Brain Research, special issue on brain injury and recovery. Brain Research, 1640 (Part A), 114-129. Doi: 10.1016/j.brainres.2015.12.30.
Peterson, T. C., Maass, W., Anderson, J. R., & Hoane, M. R. (2015). Behavioral and histological characterization of fluid percussion injury and controlled cortical impact injury to the rat sensorimotor cortex. Behavioral Brain Research, 294, 254-263. Doi: 10.1016/j.bbr.2015.08.007.
Anderson, G. D., Peterson, T. C., Vonder Haar, C., Farin, F. M., Bammler, T. K., MacDonald, J. W., Kantor, E. D., Hoane, M. R. (2015). Effect of traumatic brain injury, Erythropoietin and Anakinra on hepatic metabolizing enzymes and transporters in an experimental rodent model. The American Association of Pharmaceutical Scientists Journal, 17 (5), 1255-1267. Doi: 10.1208/s12245-015-9792-y.
Peterson, T. C., Hoane, M. R., McConomy, K. S., Farin, F. M., Bammler, T. K., MacDonald, J. W., Kantor, E. D., & Anderson, G. D. (2015). A combination therapy of nicotinamide and progesterone for functional recovery following traumatic brain injury. Journal of Neurotrauma, 32 (11), 765-779. doi: 10.1089/neu.2014.3530.
Bauer, D., Peterson, T. C., & Swain, R. A. (2014). Cerebellar dentate nuclei lesions alter prefrontal cortex dendritic spine morphology. Brain Research, 1544, 15-24. doi: 10.1016/j.brainres.2013.11.032.
Anderson, G., Peterson, T. C., Vonder Haar, C., Kantor, E. D., Farin, F. M., Bammler, T. K., Macdonald, J. W., & Hoane, M. R. (2013). Comparison of the effects of Erythropoietin and Anakinra on functional recovery and gene expression in a traumatic brain injury model. Frontiers in Neuroscience, 4 (29), 1-14. doi: 10.3389/phar.2013.00129.
Anderson, G. D., Peterson, T. C., Farin, F. M., Bammler, T. K., Beyer, R. P., Kantor, E. D., & Hoane, M. R. (2013). The effect of Nicotinamide on gene expression following traumatic brain injury. Frontiers in Neuroscience, 7 (21), 1-16. doi: 10.3389/ fnins.2013.00021
Peterson, T. C., Anderson, G., & Hoane, M. R. (2012). A comparison of the effects of nicotinamide and progesterone on functional recovery of cognitive behavior following cortical contusion injury in the rat. Journal of Neurotrauma, 29, 2823-2830. doi: 10.3389/fphar.2013.00129.
Peterson, T. C., Villatoro, L. O., Arneson, T., Ahuja, B., Voss, S., & Swain, R. (2012). Behavior modification after inactivation of the cerebellar dentate nuclei. Behavioral Neuroscience, 126, 551-562. doi: 10.1037/a0028701.
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* indicates co authorship