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Frederick Zeiler is a Canadian neurotrauma neurosurgeon currently employed as a clinician-scientist at the University of Manitoba. He completed his BSc in 2005 at the University of Manitoba, focused on applied mathematics and physical chemistry, holding National Sciences and Engineering Research Council (NSERC) summer research awards during this time. He went on to complete his medical school at the University of Manitoba, followed by his neurosurgery residency at the same institution. Dr. Zeiler has also completed dedicated fellowship training in neurocritical care at the Montreal Neurological Institute and the Royal College of Physicians and Surgeons of Canada (RCPSC) clinician investigator program at the University of Manitoba. Finally, he completed his PhD training at the University of Cambridge, with his studies focused on advanced multi-modal monitoring of cerebrovascular reactivity in adult moderate and severe TBI, under the supervision of world experts in TBI research: Prof David Menon and Prof Marek Czosnyka. During his time in Cambridge, he was recognized as both a Royal College of Surgeons of Canada Travelling Fellow in Surgery and University of Cambridge International Trust Scholar for the entirety of his studies.

Currently, he is a clinician-scientist, Assistant Professor and Director of Neurosurgery Research at the University of Manitoba, as well as clinical lead for the new cranial neurotrauma service. His newly developing research program in Winnipeg is focused on the application of multi-modal invasive/non-invasive cranial physiologic monitoring for the continuous assessment of cerebral autoregulation, compensatory reserve, autonomics and signal entropy. This program will integrate complex high-frequency signal processing, with neuroimaging, serum/CSF/microdialysis protein and genetic biomarkers. The goal is to uncover the molecular mechanisms involved in impaired cerebrovascular reactivity in TBI, leading to the development of potential therapeutic targets directed at prevention and treatment of vascular dysfunction in TBI.