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"Concordant with this fact, a research using different cellular models such as neuroblastoma SH-SY5Y and NT (2) neuronal cells shows that Abeta42 treatment downregulates UCHL-1 and this down-regulation is dependent on NF-kappaB activation and on impaired BACE1 lysosomal degradation.39 Ubiquitin C-terminal hydrolase-1 accelerates BACE1 degradation and affects APP processing and Abeta production.40 In conclusion, potentiation of UCHL-1 might be able to reduce the levels of BACE1 and Abeta in brain, and UCHL-1 may be a novel target for AD drug development."