• Daya A Grant, Rebecka Serpa, Cameron R Moattari, Ari Brown, Tiffany Greco, Mayumi L Prins, and Edmond Teng.
• 1 Department of Neurosurgery, UCLA , Los Angeles, California.
• J. Neurotrauma. 2018 Jan 1; 35 (1): 94-104.

AbstractSingle moderate-to-severe traumatic brain injuries (TBIs) may increase subsequent risk for neurodegenerative disease by facilitating β-amyloid (Aβ) deposition. However, the chronic effects on Aβ pathogenesis of repetitive mild TBIs (rTBI), which are common in adolescents and young adults, remain uncertain. We examined the effects of rTBI sustained during adolescence on subsequent deposition of Aβ pathology in a transgenic APP/PS1 rat model. Transgenic rats received sham or four individual mild TBIs (rTBIs) separated by either 24- or 72-h intervals at post-natal day 35 (before Aβ plaque deposition). Animals were euthanized at 12 months of age and underwent immunohistochemical analyses of Aβ plaque deposition. Significantly greater hippocampal Aβ plaque deposition was observed after rTBI separated by 24 h relative to rTBI separated by 72 h or sham injuries. These increases in hippocampal Aβ plaque load were driven by increases in both plaque number and size. Similar, though less-pronounced, effects were observed in extrahippocampal regions. Increases in Aβ plaque deposition were observed both ipsilaterally and contralaterally to the injury site and in both males and females. rTBIs sustained in adolescence can increase subsequent deposition of Aβ pathology, and these effects are critically dependent on interinjury interval.

21 keywords...

hide…