The council is made up of members who are survivors of brain injury, family members of individuals who have experienced a brain injury, and/or professionals working in a field related to brain injury services.
Appointed members are typically appointed to serve two-year terms, beginning in July. These will be underpinned by concordant research in animal models, which not only address mechanistic questions, but also allow direct comparison with the unique human neuropathology data in the Glasgow TBI archive, and use genetic interventions and novel compounds (provided by our industrial partners) to study the modulation of neuroinflammation.Members of the Advisory Council on Brain Injuries (ACBI) are appointed annually by the Governor of Iowa.
Our international, multidisciplinary team will explore the neuroinflammatory response in complementary clinical studies in all severities and age ranges of TBI. Translation of these experimental data to clinical TBI is limited by the paucity of human data. This is an oversimplification, but provides a conceptual framework to understand the repertoire of microglial response. Microglial activation in experimental TBI results in variable phenotypes with pro-inflammatory or wound healing/anti-inflammatory roles, often classified as M1 or M2 responses. Recent interest has focused on the adaptive immune response after experimental neurotrauma, but data on its impact are conflicting. Neuropathology and positron emission tomography suggest persistent microglial activation years after TBI, but such cross-sectional analyses cannot determine whether neuroinflammation drives ongoing neuronal loss.
Neuroinflammation is mechanistically important in traumatic brain injury (TBI), may persist for years following ictus, could contribute to late cognitive decline, and might explain how TBI is an epigenetic driver for late neurodegeneration.