Cerebral amyloid-β accumulation and deposition following traumatic brain injury—A narrative review and meta-analysis of animal studiesNeuroscience & Biobehavioral Reviews (2016)
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.
- Traumatic brain injury,
- Alzheimer’s disease,
- Animal models,
Publication DateMay, 2016
Citation InformationSabine M Bird, Hamid R Sohrabi, Thomas A Sutton, Michael Weinborn, et al.. "Cerebral amyloid-β accumulation and deposition following traumatic brain injury—A narrative review and meta-analysis of animal studies" Neuroscience & Biobehavioral Reviews Vol. 64 (2016) p. 215 - 228
Available at: http://works.bepress.com/leigh-patterson/1/