The objective of the present study was to examine the role of selenium in the metabolism of Aβ and in Aβ-induced neuronal death. Selenium treatment significantly reduced Aβ40, Aβ42, and sAPPβ production by reducing Aβ producing β-secretase and γ-secretase activities. The lipid peroxidation product 4-Hydroxynonenal (HNE)-induced transcription of β-secretase (BACE1) was blocked by selenium. Finally, our data show that selenium protects against HNE and Aβ-mediated toxicity in primary cultured neurons. The present study suggests that selenium may be able to salvage the neuronal degeneration of Alzheimer's disease, thereby limiting β-amyloid production and neuronal death.
- Alzheimer's disease
- Lipid peroxidation