title: Traumatic brain injury and amyloid-β pathology: a link to Alzheimer's disease?
abstract: Traumatic brain injury (TBI) has devastating acute effects and in many cases seems to initiate long-term neurodegeneration. Indeed, an epidemiological association between TBI and the development of Alzheimer's disease (AD) later in life has been demonstrated, and it has been shown that amyloid-β (Aβ) plaques — one of the hallmarks of AD — may be found in patients within hours following TBI. Here, we explore the mechanistic underpinnings of the link between TBI and AD, focusing on the hypothesis that rapid Aβ plaque formation may result from the accumulation of amyloid precursor protein in damaged axons and a disturbed balance between Aβ genesis and catabolism following TBI.
authors.affiliation: Brain Injury and Repair, Departmentof Neurosurgery, University of Pennsylvania School of Medicine, 3320 Smith Walk, Hayden Hall 105, Philadelphia, Pennsylvania 19104, USA; University of Glasgow, University Avenue, Glasgow G12 8QQ, UK.
authors.forename: Victoria E
authors.initials: VE
authors.lastname: Johnson
authors.forename: William
authors.initials: W
authors.lastname: Stewart
authors.forename: Douglas H
authors.initials: DH
authors.lastname: Smith
mesh_terms: D000544:Alzheimer Disease / Q000209:etiology / Q000378:metabolism / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D001369:Axons / Q000378:metabolism / Q000473:pathology; D001921:Brain / Q000378:metabolism / Q000473:pathology*; D001930:Brain Injuries / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D058225:Plaque, Amyloid / Q000473:pathology*
chemical_list: D016229:Amyloid beta-Peptides