Age moderates the effects of traumatic brain injury on beta-amyloid plaque load in APP/PS1 mice

Traumatic brain injury (TBI) has been identified as a risk factor for Alzheimer's disease (AD). However, how such neural damage contributes to AD pathology remains unclear; specifically, the relationship between the timing of a TBI relative to ageing and the onset of AD pathology is not known. In this study, we have examined the effect of TBI on subsequent beta-amyloid (Aβ) deposition in APP/PS1 (APPSWE/PSEN1dE9) transgenic mice either before (3 months of age) or after the onset (6 months of age) of plaque pathology. Lateral fluid percussion (LFPI), a model of diffuse brain injury, was induced in APP/PS1 and C57Bl/6 wild-type littermates (WT). LFPI caused a significant increase in both total (pppp>0.05), Aβ plaque load compared to sham treated mice. No Aβ plaques were present in any WT mice across these conditions. GFAP-immunolabelling of astrocytes and Iba-1-immunolabelling of microglial/macrophages was not significantly different (pβ plaque deposition depending on age and the stage of amyloidosis at the time of injury