Cerebral amyloid-β accumulation and deposition following traumatic brain injury—A narrative review and meta-analysis of animal studies. (May 2016)

• Record Type: Journal Article
• 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.
• Is Part Of: Neuroscience and biobehavioral reviews. Volume 64(2016)
• Page Start: 215
• Page End: 228
• Publication Date: 2016-05
• Subjects: Traumatic brain injury -- TBI -- Amyloid-β -- Alzheimer's disease -- Animal models -- dementia; Psychophysiology -- Periodicals; Human behavior -- Periodicals; Animal behavior -- Periodicals; Neurology -- Periodicals; Behavior -- Periodicals; Ethology -- Periodicals; Neurology -- Periodicals; Psychophysiologie -- Périodiques; Comportement humain -- Périodiques; Animaux -- Mœurs et comportement -- Périodiques; Neurologie -- Périodiques; Animal behavior; Human behavior; Neurology; Psychophysiology; Periodicals; Electronic journals; 573.8
• DOI: 10.1016/j.neubiorev.2016.01.004
• Languages: English
• ISSNs: 0149-7634

Abstract

Highlights: Animal studies show an acute, significant increase of Aβ following brain injury. Few studies assessing longer-term Aβ-levels show a reduction over a period of weeks. There is a critical need for standardized, experimental methods and bigger samples sizes. New imaging techniques may improve the accuracy of Aβ detection in animal studies. Abstract: 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 24 h to one month following TBI (overall log OR = 2.97 ± 0.40, p < 0.001). These findings may contribute to further understanding the relationship between TBI and future dementia risk. The methodological inconsistencies of the studies discussed in this review suggest the need for improved and more standardised data collection and study design, in order to properly elucidate the role of TBI in the expression and accumulation of Aβ.