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While classic theories\nsuggest that traumatically injured axons are mechanically torn at the moment of\ninjury, studies in the last two decades have not supported this premise in the\nmajority of injured axons. Rather, current thought considers TAI a progressive\nprocess evoked by the tensile forces of injury, gradually evolving from focal\naxonal alteration to ultimate disconnection. Recent observations have\ndemonstrated that traumatically induced focal axolemmal permeability leads to\nlocal influx of Ca2+ with the subsequent activation of the cysteine proteases,\ncalpain and caspase, that then play a pivotal role in the ensuing pathogenesis of\nTAI via proteolytic digestion of brain spectrin, a major constituent of the\nsubaxolemmal cytoskeletal network, the \"membrane skeleton\". In this pathological \nprogression this local Ca2+ overloading with the activation of calpains also\ninitiates mitochondrial injury that results in the release of cytochrome-c, with \nthe activation of caspase. Both the activated calpain and caspases then\nparticipate in the degradation of the local axonal cytoskeleton causing local\naxonal failure and disconnection. In this review, we summarize contemporary\nthought on the pathogenesis of TAI, while discussing the potential diversity of\npathological processes observed within various injured fiber types. The\nanterograde and retrograde consequences of TAI are also considered together with \na discussion of various experimental therapeutic approaches capable of\nattenuating TAI.", "subjects" : [ { "otype" : "Classification", "mtid" : 12215, "link" : "/api/classification/12215", "label" : "Klinikai orvostan", "published" : true, "snippet" : true } ], "digital" : null, "printed" : null, "sourceYear" : 2009, "foreignEdition" : true, "foreignLanguage" : true, "fullPublication" : true, "conferencePublication" : false, "nationalOrigin" : true, "missingAuthor" : false, "oaType" : "NONE", "oaCheckDate" : "2024-03-08", "oaFree" : false, "citationCount" : 440, "citationCountUnpublished" : 0, "citationCountWoOther" : 437, "independentCitCountWoOther" : 423, "nationalOriginCitationCount" : 3, "foreignEditionCitationCount" : 404, "doiCitationCount" : 419, "wosCitationCount" : 379, "scopusCitationCount" : 425, "wosScopusCitationCount" : 437, "wosScopusCitationCountWoOther" : 437, 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