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Treatment is effective for only 60%\u201070% of patients and remains symptomatic despite decades of effort to develop epilepsy prevention therapies. Recent preclinical efforts are focused on likely primary drivers of epileptogenesis, namely inflammation, neuron loss, plasticity, and circuit reorganization. This review suggests a path to identify neuronal and molecular targets for clinical testing of specific hypotheses about epileptogenesis and its prevention or modification. Acquired human epilepsies with different etiologies share some features with animal models. We identify these commonalities and discuss their relevance to the development of successful epilepsy prevention or disease modification strategies. Risk factors for developing epilepsy that appear common to multiple acute injury etiologies include intracranial bleeding, disruption of the blood\u2010brain barrier, more severe injury, and early seizures within 1 week of injury. In diverse human epilepsies and animal models, seizures appear to propagate within a limbic or thalamocortical\/corticocortical network. Common histopathologic features of epilepsy of diverse and mostly focal origin are microglial activation and astrogliosis, heterotopic neurons in the white matter, loss of neurons, and the presence of inflammatory cellular infiltrates. Astrocytes exhibit smaller K\n                    <jats:sup>+<\/jats:sup>\n                    conductances and lose gap junction coupling in many animal models as well as in sclerotic hippocampi from temporal lobe epilepsy patients. There is increasing evidence that epilepsy can be prevented or aborted in preclinical animal models of acquired epilepsy by interfering with processes that appear common to multiple acute injury etiologies, for example, in post\u2013status epilepticus models of focal epilepsy by transient treatment with a trkB\/\n                    <jats:styled-content style=\"fixed-case\">PLC<\/jats:styled-content>\n                    \u03b31 inhibitor, isoflurane, or\n                    <jats:styled-content style=\"fixed-case\">HMGB<\/jats:styled-content>\n                    1 antibodies and by topical administration of adenosine, in the cortical fluid percussion injury model by focal cooling, and in the albumin posttraumatic epilepsy model by losartan. Preclinical studies further highlight the roles of\n                    <jats:styled-content style=\"fixed-case\">mTOR<\/jats:styled-content>\n                    1 pathways,\n                    <jats:styled-content style=\"fixed-case\">JAK<\/jats:styled-content>\n                    \u2010\n                    <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>\n                    3,\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20101R\/\n                    <jats:styled-content style=\"fixed-case\">TLR<\/jats:styled-content>\n                    4 signaling, and other inflammatory pathways in the genesis or modulation of epilepsy after brain injury. The wealth of commonalities, diversity of molecular targets identified preclinically, and likely multidimensional nature of epileptogenesis argue for a combinatorial strategy in prevention therapy. Going forward, the identification of impending epilepsy biomarkers to allow better patient selection, together with better alignment with multisite preclinical trials in animal models, should guide the clinical testing of new hypotheses for epileptogenesis and its prevention.\n                  <\/jats:p>","DOI":"10.1111\/epi.13965","type":"journal-article","created":{"date-parts":[[2017,12,16]],"date-time":"2017-12-16T17:07:16Z","timestamp":1513444036000},"page":"37-66","source":"Crossref","is-referenced-by-count":268,"title":["Commonalities in epileptogenic processes from different acute brain insults: Do they translate?"],"prefix":"10.1111","volume":"59","author":[{"given":"Pavel","family":"Klein","sequence":"first","affiliation":[{"name":"Mid\u2010Atlantic Epilepsy and Sleep Center Bethesda MD USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Raymond","family":"Dingledine","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Emory University Atlanta GA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eleonora","family":"Aronica","sequence":"additional","affiliation":[{"name":"Department of (Neuro) Pathology Academic Medical Center and Swammerdam Institute for Life Sciences Center for Neuroscience University of Amsterdam Amsterdam The Netherlands"},{"name":"Stichting Epilepsie Instellingen Nederland (SEIN) Heemstede The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3014-1966","authenticated-orcid":false,"given":"Christophe","family":"Bernard","sequence":"additional","affiliation":[{"name":"Aix Marseille Univ, Inserm, INS, Instit Neurosci Syst Marseille 13005 France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8676-0788","authenticated-orcid":false,"given":"Ingmar","family":"Bl\u00fcmcke","sequence":"additional","affiliation":[{"name":"Department of Neuropathology University Hospital Erlangen Erlangen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Detlev","family":"Boison","sequence":"additional","affiliation":[{"name":"Robert Stone Dow Neurobiology Laboratories Legacy Research Institute Portland OR USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1781-2892","authenticated-orcid":false,"given":"Martin J.","family":"Brodie","sequence":"additional","affiliation":[{"name":"Epilepsy Unit West Glasgow Ambulatory Care Hospital\u2010Yorkhill Glasgow UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Amy R.","family":"Brooks\u2010Kayal","sequence":"additional","affiliation":[{"name":"Division of Neurology Departments of Pediatrics and Neurology, University of Colorado School of Medicine Aurora CO USA"},{"name":"Children's Hospital Colorado Aurora CO USA"},{"name":"Neuroscience Program University of Colorado Anschutz Medical Campus Aurora CO USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"suffix":"Jr","given":"Jerome","family":"Engel","sequence":"additional","affiliation":[{"name":"Departments of Neurology, Neurobiology, and Psychiatry and Biobehavioral Sciences David Geffen School of Medicine Brain Research Institute University of California Los Angeles CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Patrick A.","family":"Forcelli","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Georgetown University Washington DC USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lawrence J.","family":"Hirsch","sequence":"additional","affiliation":[{"name":"Department of Neurology Yale University New Haven CT USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rafal M.","family":"Kaminski","sequence":"additional","affiliation":[{"name":"UCB Pharma Braine\u2010l'Alleud Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Henrik","family":"Klitgaard","sequence":"additional","affiliation":[{"name":"UCB Pharma Braine\u2010l'Alleud Belgium"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katja","family":"Kobow","sequence":"additional","affiliation":[{"name":"Department of Neuropathology University Hospital Erlangen Erlangen Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel H.","family":"Lowenstein","sequence":"additional","affiliation":[{"name":"Department of Neurology University of California San Francisco CA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Phillip L.","family":"Pearl","sequence":"additional","affiliation":[{"name":"Department of Neurology Boston Children's Hospital Harvard Medical School Boston MA USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Asla","family":"Pitk\u00e4nen","sequence":"additional","affiliation":[{"name":"Department of Neurobiology A. 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