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1 Department of Neuroscience, Central Clinical School, Monash University, The Alfred Hospital, Melbourne, Australia; Department of Medicine (Royal Melbourne Hospital), The University of Melbourne, Melbourne, Australia.
2 Department of Neuroscience, Central Clinical School, Monash University, The Alfred Hospital, Melbourne, Australia; Department of Medicine (Royal Melbourne Hospital), The University of Melbourne, Melbourne, Australia. Electronic address: te.obrien@alfred.org.au.
1 Department of Neuroscience, Central Clinical School, Monash University, The Alfred Hospital, Melbourne, Australia; Department of Medicine (Royal Melbourne Hospital), The University of Melbourne, Melbourne, Australia.
2 Department of Neuroscience, Central Clinical School, Monash University, The Alfred Hospital, Melbourne, Australia; Department of Medicine (Royal Melbourne Hospital), The University of Melbourne, Melbourne, Australia. Electronic address: te.obrien@alfred.org.au.
In the quest for developing new therapeutic targets for post-traumatic epilepsies (PTE), identifying mechanisms relevant to development and progression of disease is critical. A growing body of literature suggests involvement of neurodegenerative mechanisms in the pathophysiology of acquired epilepsies, including following traumatic brain injury (TBI). In this review, we discuss the potential of some of these mechanisms to be targets for the development of a therapy against PTE.
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