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We previously demonstrated that damage to the central auditory pathway resulting from blast\u2010induced TBI (bTBI) could be significantly attenuated by a combinatorial antioxidant treatment regimen.  In the current study, we examined the localization patterns of normal Tau and the potential blast\u2010induced accumulation of neurotoxic variants of this microtubule\u2010associated protein that are believed to potentiate the neurodegenerative effects associated with synaptic dysfunction in the hippocampus following three successive blast overpressure exposures in nontransgenic rats. We observed a marked increase in the number of both hyperphosphorylated and oligomeric Tau\u2010positive hilar mossy cells and somatic accumulation of endogenous Tau in oligodendrocytes in the hippocampus. Remarkably, a combinatorial regimen of 2,4\u2010disulfonyl <jats:italic>\u03b1<\/jats:italic>\u2010phenyl tertiary butyl nitrone (HPN\u201007) and <jats:italic>N<\/jats:italic>\u2010acetylcysteine (NAC) resulted in striking reductions in the numbers of both mossy cells and oligodendrocytes positively labeled for these pathological Tau immunoreactivity patterns  in response to bTBI. This treatment strategy represents a promising therapeutic approach for simultaneously reducing or eliminating both primary auditory injury and nonauditory changes associated with bTBI\u2010induced hippocampal neurodegeneration.<\/jats:p>","DOI":"10.1155\/2016\/4159357","type":"journal-article","created":{"date-parts":[[2015,12,17]],"date-time":"2015-12-17T07:15:27Z","timestamp":1450336527000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":35,"title":["Ameliorative Effects of Antioxidants on the Hippocampal Accumulation of Pathologic Tau in a Rat Model of Blast\u2010Induced Traumatic Brain Injury"],"prefix":"10.1155","volume":"2016","author":[{"given":"Xiaoping","family":"Du","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthew 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