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However, critical knowledge gaps remain regarding underlying mechanisms (e.g. de novo protein synthesis, changes in barrier permeabilities and\/or glymphatic clearance), especially for \u201cmilder\u201d injuries. Multiple experiments (\n                    <jats:italic toggle=\"yes\">N<\/jats:italic>\n                    \u2009=\u200952 swine) used precise, biomechanical targeting of three \u201cmild-to-moderate\u201d TBI levels, pharmacological manipulation of blood\u2013brain barrier permeability (mannitol bolus), and dense temporal sampling of hyper-acute and acute phases to characterize protein kinetics and underlying mechanisms. Glial fibrillary acidic protein (GFAP) and neurofilament light (NfL) exhibited dose-dependent relationships with precisely quantified biomechanics, which respectively varied in terms of early (minutes to hours post-injury; GFAP) versus late (1-week post-injury; NfL) peak efflux. Mannitol administration replicated trauma-related kinetics of protein release during hyper-acute to acute phases, implicating blood\u2013brain barrier breach as a primary mechanism, and potentially suggesting that efflux timing is partially mediated by molecular weight. Immunohistochemical evidence (Immunoglobulin G) exhibited similar dose-dependent evidence of blood\u2013brain barrier breach, with spatial deposition patterns that varied across TBI (increased in sulcal fundi\/deep gray matter) versus mannitol (diffuse deposition) models. Findings collectively suggest multiple, non-exclusive mechanisms which mediate post-traumatic protein efflux, and that commercially available proteomics may dynamically quantify blood\u2013brain barrier integrity.\n                  <\/jats:p>","DOI":"10.1177\/0271678x261432754","type":"journal-article","created":{"date-parts":[[2026,4,4]],"date-time":"2026-04-04T10:54:50Z","timestamp":1775300090000},"page":"2174-2186","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":1,"title":["Mechanisms and barriers for understanding neural abundant protein efflux following traumatic brain injury"],"prefix":"10.1177","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-2396-5609","authenticated-orcid":false,"given":"Andrew R","family":"Mayer","sequence":"first","affiliation":[{"name":"The Mind Research Network\/Lovelace Biomedical Research Institute, Pete &amp; Nancy Domenici Hall, Albuquerque, NM, 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