Cerebral amyloid-β accumulation and deposition following traumatic brain injury--A narrative review and meta-analysis of animal studies

• Published in: Neuroscience and biobehavioral reviews 2016-05, Vol.64, p.215-228
• Main Authors: Bird, Sabine M, Sohrabi, Hamid R, Sutton, Thomas A, Weinborn, Michael, Rainey-Smith, Stephanie R, Brown, Belinda, Patterson, Leigh, Taddei, Kevin, Gupta, Veer, Carruthers, Malcolm, Lenzo, Nat, Knuckey, Neville, Bucks, Romola S, Verdile, Giuseppe, Martins, Ralph N
• Format: Article
• Language: English
• Subjects: Amyloid beta-Peptides - metabolism; Animals; Brain - metabolism; Brain Injuries, Traumatic - metabolism; Humans
• ISSN: 0149-7634; 1873-7528
• DOI: 10.1016/j.neubiorev.2016.01.004

Traumatic brain injury (TBI) increases the risk of neurodegenerative disorders many years post-injury. However, molecular mechanisms underlying the relationship between TBI and neurodegenerative diseases, such as Alzheimer's disease (AD), remain to be elucidated. Nevertheless, previous studies have demonstrated a link between TBI and increased amyloid-β (Aβ), a protein involved in AD pathogenesis. Here, we review animal studies that measured Aβ levels following TBI. In addition, from a pool of initially identified 1209 published papers, we examined data from 19 eligible animal model studies using a meta-analytic approach. We found an acute increase in cerebral Aβ levels ranging from 24h to one month following TBI (overall log OR=2.97 ± 0.40, p