Role of APOE Isforms in the Pathogenesis of TBI Induced Alzheimer's Disease.

摘要

During the reported period, we have been able to optimize the conditions for CCI. The goal of the optimization was to avoid overshooting, to diminish the depth of the impact and thus to reproducibly obtain and process brain tissue with minimal necrotic changes as close as possible to the impact. The experimental groups for both SAs are being generated. However, unexpectedly Abca1 knockout mice on human APOE genetic background were exceptionally difficult to generate. We are considering changes in the genotype of those particular groups, which has been mentions in the alternatives of the original proposal. The pilot mRNA-seq experiments are completed. The results demonstrated that metabolic and regulatory pathways relevant to inflammatory and immune reactions (of particular importance genes like Trem2 and Tyrobp), as well as Amyloid-beta clearance critical for immediate and long term response to TBI can be modulated efficiently.