Daniel Fulton is a Birmingham Fellow in the Neurotrauma and Neurodegeneration section of the School of Clinical and Experimental Medicine. Dr Fulton also holds an honorary appointment at the School of Life Science at the University of Warwick through his role as a Senior Research Fellow in the Science Cities Research Alliance.
Daniel obtained his PhD in Neuroscience at the University of Sussex in 2003 where his thesis focused on the cellular mechanisms of learning and memory. Following his PhD he pursued postdoctoral research at the University of California Los Angeles (UCLA) where he continued to work on synaptic plasticity and learning and memory. In 2007 he joined the lab of Anthony Campagnoni (also at UCLA) where he begun his work on glial biology. Daniel’s work as a Research Neuroscientist in the Campagnoni lab focused on the physiological properties of oligodendrocytes and the expression of novel myelin proteins within striatal neurons. In 2010 Daniel was awarded a Senior Fellowship with the Science City Research Alliance and in 2011 he obtained a Marie Curie Career Integration Grant. Using these fellowships Daniel returned to the UK to pursue independent work at the University of Warwick investigating the role of neuronal activityin oligodendrocyte development and myelin formation. In July 2013 Daniel moved to the University of Birmingham to take up an appointment as a Birmingham Fellow where he is establishing a Glial Biology group within the Neurotrauma and Neurodegeneration section of the School of Clinical and Experimental Medicine.
Work within the Glial Biology group will continue to explore activity-dependent mechanisms controlling myelin formation and repair while also establishing new lines of research to complement the neurotrauma and repair work underway within the Neurotrauma and Neurodegeneration Section.
Dr Fulton studies the role of neuronal activity in guiding the development and repair of myelin in the central nervous system (CNS). This insulating material enwraps axons speeding the conduction of nerve impulses between distantly located brain regions. Damage to myelin through traumatic injury and disease disturbs the coordinated flow of information throughout the CNS and leading to impairments in cognition and movement. Therefore understanding the mechanisms by which neuronal activity promotes myelin formation and repair could have useful applications in the context of myelin replacement for individuals bearing myelin loss through disease and traumatic injury.