{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T19:03:19Z","timestamp":1790017399812,"version":"4.0.1"},"reference-count":48,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2017,6,19]],"date-time":"2017-06-19T00:00:00Z","timestamp":1497830400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Brain Pathology"],"published-print":{"date-parts":[[2018,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Deposition of amyloid\u2010\u03b2 (A\u03b2) is central to Alzheimer's disease (AD) pathogenesis and associated with progressive neurodegeneration in traumatic brain injury (TBI). We analyzed predisposing factors for A\u03b2 deposition including monomeric A\u03b240, A\u03b242 and A\u03b2 oligomers\/protofibrils, A\u03b2 species with pronounced neurotoxic properties, following human TBI. Highly selective ELISAs were used to analyze N\u2010terminally intact and truncated A\u03b240 and A\u03b242, as well as A\u03b2 oligomers\/protofibrils, in human brain tissue, surgically resected from severe TBI patients (<jats:italic>n<\/jats:italic>\u2009=\u200912; mean age 49.5\u2009\u00b1\u200919 years) due to life\u2010threatening brain swelling\/hemorrhage within one week post\u2010injury. The TBI tissues were compared to post\u2010mortem AD brains (<jats:italic>n<\/jats:italic>\u2009=\u20095), to post\u2010mortem tissue of neurologically intact (NI) subjects (<jats:italic>n<\/jats:italic>\u2009=\u20094) and to cortical biopsies obtained at surgery for idiopathic normal pressure hydrocephalus patients (iNPH; <jats:italic>n<\/jats:italic>\u2009=\u20094). The levels of A\u03b240 and A\u03b242 were not elevated by TBI. The levels of A\u03b2 oligomers\/protofibrils in TBI were similar to those in the significantly older AD patients and increased compared to NI and iNPH controls (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05). Moreover, TBI patients carrying the AD risk genotype Apolipoprotein E epsilon3\/4 (APOE <jats:italic>\u03b5<\/jats:italic>3\/4; <jats:italic>n<\/jats:italic>\u2009=\u20094) had increased levels of A\u03b2 oligomers\/protofibrils (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05) and of both N\u2010terminally intact and truncated A\u03b242 (<jats:italic>P<\/jats:italic>\u2009&lt;\u20090.05) compared to APOE <jats:italic>\u03b5<\/jats:italic>3\/4\u2010negative TBI patients (<jats:italic>n<\/jats:italic>\u2009=\u20098). Neuropathological analysis showed insoluble A\u03b2 aggregates (commonly referred to as A\u03b2 plaques) in three TBI patients, all of whom were APOE <jats:italic>\u03b5<\/jats:italic>3\/4 carriers. We conclude that soluble intermediary A\u03b2 aggregates form rapidly after TBI, especially among APOE <jats:italic>\u03b5<\/jats:italic>3\/4 carriers. Further research is needed to determine whether these aggregates aggravate the clinical short\u2010 and long\u2010term outcome in TBI.<\/jats:p>","DOI":"10.1111\/bpa.12532","type":"journal-article","created":{"date-parts":[[2017,5,29]],"date-time":"2017-05-29T23:52:41Z","timestamp":1496101961000},"page":"451-462","source":"Crossref","is-referenced-by-count":39,"title":["Rapid amyloid\u2010\u03b2 oligomer and protofibril accumulation in traumatic brain injury"],"prefix":"10.1111","volume":"28","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6173-8357","authenticated-orcid":false,"given":"Sami","family":"Abu Hamdeh","sequence":"first","affiliation":[{"name":"Department of Neuroscience, Section of Neurosurgery Uppsala University Uppsala Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Erik Rollman","family":"Waara","sequence":"additional","affiliation":[{"name":"BioArctic Neuroscience AB Stockholm 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