Lab website: www.brennanresearchlab.com
2020-2022: Research Scientist, The Ohio State University, USA
2016-2020: Post-doctoral fellow, The Ohio State University, USA
2011-2015: Ph.D. in Physiology, The University of Queensland, Australia
2010: B.Sc. Hons (Class I) The University of Queensland, Australia
2007-2009: B.Sc. in Medical Science, The University of Queensland, Australia
2021-2023: Chronic Brain Injury Program Pilot Award
2021-2022: Neuroscience Research Institute Grant
2021: EBIC Sir Graham Teasdale Award, International Neurotrauma Society
2020: Post-doctoral Scholar Mentor of the Year Award
2020: Fritz Seil award, International Society for Neural Regeneration
2019-2022: Wings for Life Fellowship
2017-2019: Craig H. Neilsen Postdoctoral Fellowship
2016: Career Development Grant
2015: Research Travel Fellowship
2015: Dean's award for Outstanding Ph.D. Thesis
2011-2015: Australian Postgraduate Award
2011: Establishment Grant
Please visit our lab website: www.brennanresearchlab.com for project information.
The Brennan Lab is part of the Department of Biomedical & Molecular Sciences (DBMS). Our lab space is situated on the 7th floor of Botterell Hall. The Brennan Lab is actively recruiting students, postdoctoral fellows and Research Assistants with backgrounds in biology, neuroscience, immunology, genomics, bioinformatics, or related sciences who are interested in pursuing further training.
1. Neuroinflammation after neurotrauma
Trauma to the brain or spinal cord triggers a robust neuro-inflammatory response. The cells involved in this response include tissue-resident glia (e.g. microglia, astrocytes) and infiltrating immune cells (e.g. neutrophils, monocyte-derived macrophages, lymphocytes). Discovery projects in this theme seek to understand how these cells communicate with neurons, each other, and the lesion microenvironment to coordinate tissue repair and recovery of function, or secondary injury pathology and poor injury outcomes.
2. Peripheral complications after neurotrauma
Trauma to the spinal cord can cause morbidity in peripheral systems, particularly in primary and secondary lymphoid tissues. Discovery projects in this theme seek to understand how events and morbidities that impact peripheral immune organs shape outcomes from spinal cord injury, and vice versa.
Please visit our lab website: www.brennanresearchlab.com for a full list of publications.
Brennan, F.H., Li, Y., Wang, C., Ma, A., Guo, Q., Li, Y., Pukos, N., Campbell, W.A., Witcher, K.G., Guan, Z., Kigerl, K.A., Hall, J.C.E, Godbout, J.P., Fischer, A.J., McTigue, D.M., He, Z., Ma, Q. and Popovich, P.G. 2022. Microglia coordinate cellular interactions during spinal cord repair in mice. Nature Communications, 13, 4096
Du, Y*, Brennan, F.H.*, Popovich, P.G, and Zhou, M. 2022. Microglia maintain the normal structure and function of the hippocampal astrocyte network Glia, 70:1359-1379 *Co-first authors
Noble, B.T.*, Brennan, F.H.*, Wang, Y., Guan, Z., Mo, X, Schwab, J.M., and Popovich, P.G. 2022. Thoracic VGlut2+ spinal interneurons regulate structural and functional plasticity of sympathetic networks after high-level spinal cord injury. The Journal of Neuroscience, 42(17):3659-3675 *Co-first authors
Brennan, F.H.*, Noble, B.T.*, Wang, Y.* Guan, Z, Davis, H., Mo, X., Harris, C., Eroglu, C., Ferguson, A.R., and Popovich, P.G. 2021. Acute post-injury blockade of α2δ-1 calcium channel subunits prevents pathological autonomic plasticity after spinal cord injury. Cell Reports, 34(4):108667 *Co-first authors
Freria, C.M., Brennan, F.H., Sweet, D.R., Guan, Z., Hall, J.C., Kigerl, K.A., Nemeth, D., Liu, X., Lacroix, S., Quan, N., and Popovich, P.G. 2020. Serial systemic injections of endotoxin (LPS) elicit neuroprotective spinal cord microglia through IL-1-dependent cross-talk with endothelial cells. The Journal of Neuroscience, 40 (47): 9103-2120.
Carpenter, R.S., Marbourg, J., Brennan, F.H., Mifflin, K.A., Hall, J., Jiang, R., Mo, X., Karunasiri, M., Burke, M., Dorrance, A., and Popovich, P.G. 2020. Spinal cord injury causes chronic bone marrow failure. Nature Communications, 11(3702); 1-13.
Brennan, F.H. and Popovich, P.G. 2018. Emerging targets for reprograming the immune response to promote repair and recovery of function after spinal cord injury. Current Opinion in Neurology, 31(3):334-44
Brennan, F.H., Jogia, T., Gillespie, E.R., Blomster, L.V., Li, X., Nowlan, B., Williams, G.M., Jacobson, El., Osborne, G.W., Meunier, F.A., Taylor, S.M., Campbell, K.E., MacDonald, K.P.A., Levesque, J-P., Woodruff, T.M., and Ruitenberg, M.J. 2019. Complement receptor C3aR1 controls neutrophil mobilization following spinal cord injury through physiological antagonism of CXCR2. Journal of Clinical Investigation Insight, 4(9):e98254.
Brennan, F.H., Kurniawan, N.D., Vukovic, J., Bartlett, P.F., Kasermann F., Arumugam, T.V., Basta, M., and Ruitenberg, M.J. 2016. IVIg attenuates complement and improves spinal cord injury outcomes in mice. Annals of Clinical and Translational Neurology, 3:495-511.
Brennan, F.H., Gordon, R., Lao, H.W., Biggins, P.J., Taylor, S.M., Franklin, R.J., Woodruff., T.M., and Ruitenberg., M.J. 2015. The complement receptor C5aR controls acute inflammation and astrogliosis following spinal cord injury. The Journal of Neuroscience, 35:6517-31.