{"entity": "publication", "iuid": "0cad8922da744e55b04256532548017c", "timestamp": "2026-09-25T06:04:33.209Z", "links": {"self": {"href": "https://publications-affiliated.scilifelab.se/publication/0cad8922da744e55b04256532548017c.json"}, "display": {"href": "https://publications-affiliated.scilifelab.se/publication/0cad8922da744e55b04256532548017c"}}, "title": "Intranasal Administration of the Antisecretory Peptide AF-16 Reduces Edema and Improves Cognitive Function Following Diffuse Traumatic Brain Injury in the Rat.", "authors": [{"family": "Clausen", "given": "Fredrik", "initials": "F"}, {"family": "Hansson", "given": "Hans-Arne", "initials": "HA"}, {"family": "Raud", "given": "Johan", "initials": "J"}, {"family": "Marklund", "given": "Niklas", "initials": "N"}], "type": "journal article", "published": "2017-02-14", "journal": {"title": "Front Neurol", "issn": "1664-2295", "volume": "8", "pages": "39", "issn-l": "1664-2295"}, "abstract": "A synthetic peptide with antisecretory activity, antisecretory factor (AF)-16, improves injury-related deficits in water and ion transport and decreases intracranial pressure after experimental cold lesion injury and encephalitis although its role in traumatic brain injury (TBI) is unknown. AF-16 or an inactive reference peptide was administrated intranasally 30 min following midline fluid percussion injury (mFPI; n = 52), a model of diffuse mild-moderate TBI in rats. Sham-injured (n = 14) or na\u00efve (n = 24) animals were used as controls. The rats survived for either 48 h or 15 days post-injury. At 48 h, the animals were tested in the Morris water maze (MWM) for memory function and their brains analyzed for cerebral edema. Here, mFPI-induced brain edema compared to sham or na\u00efve controls that was significantly reduced by AF-16 treatment (p < 0.05) although MWM performance was not altered. In the 15-day survival groups, the MWM learning and memory abilities as well as histological changes were analyzed. AF-16-treated brain-injured animals shortened both MWM latency and swim path in the learning trials (p < 0.05) and improved probe trial performance compared to brain-injured controls treated with the inactive reference peptide. A modest decrease by AF-16 on TBI-induced changes in hippocampal glial acidic fibrillary protein (GFAP) staining (p = 0.11) was observed. AF-16 treatment did not alter any other immunohistochemical analyses (degenerating neurons, beta-amyloid precursor protein (\u03b2-APP), and Olig2). In conclusion, intranasal AF-16-attenuated brain edema and enhanced visuospatial learning and memory following diffuse TBI in the rat. Intranasal administration early post-injury of a promising neuroprotective substance offers a novel treatment approach for TBI.", "doi": "10.3389/fneur.2017.00039", "pmid": "28261150", "labels": [], "xrefs": [{"db": "pmc", "key": "PMC5306199"}], "notes": [], "created": "2026-09-23T12:38:49.792Z", "modified": "2026-09-23T12:38:49.821Z"}