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Updated: May 26, 2026

Saccharomyces cerevisiae Models of Alzheimer's Disease to Screen Genes, Mutations, and Chemicals Affecting Amyloid Beta Production by γ-Secretase
Published on: June 24, 2025
Peroxiredoxin I regulates the component expression of γ-secretase complex causing the Alzheimer's disease
Young Ju Lee1, Jun Seo Goo, Ji Eun Kim
1Department of Biomaterials Science, College of Natural Resources and Life Science, Pusan National University, Miryang, Korea.
Abstract:
Peroxiredoxin I (Prx I) is a member of the peroxiredoxins (Prxs) family, which are antioxidant enzymes that regulate various cellular process via intracellular oxidative signal pathways. In order to investigate the correlation between Prx I and the γ-secretase complex, which causes Alzheimer's disease (AD), the expression level of Prx I was firstly evaluated in an animal model for AD. NSE/hPen-2 transgenic (Tg) mice, which were used as animal model in this study, showed a high level of Pen-2 expression and accumulation of Aβ-42 peptides in the hippocampus of brain. The expression level of Prx I was significantly higher on the mRNA and protein level in the brain of this model, while not change in Prx VI expression was observed. Furthermore, to verify the effect of Prx I on the γ-secretase components in vitro, the expression level of these components was analyzed in the Prx I transfectants. Of the components of the γ-secretase complex, the expression of PS-2 and Pen-2 was lower in the transfectants overexpressing Prx I compared to the vector transfectants. However, the expression of APP, NCT and APH-1 did not change in Prx I transfectants. Therefore, these results suggested that the expression of Prx I may be induced by the accumulation of Aβ-42 peptides and the overexpression of Prx I in neuroblastoma cells may regulate the expression of γ-secretase components.
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