Home > Publications Database > Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits induced by hippocampal injury and aging. |
Journal Article | DZNE-2022-00050 |
; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ; ;
2022
Cell Press
Cambridge, Mass.
This record in other databases:
Please use a persistent id in citations: doi:10.1016/j.cmet.2022.01.005
Abstract: Although the neurogenesis-enhancing effects of exercise have been extensively studied, the molecular mechanisms underlying this response remain unclear. Here, we propose that this is mediated by the exercise-induced systemic release of the antioxidant selenium transport protein, selenoprotein P (SEPP1). Using knockout mouse models, we confirmed that SEPP1 and its receptor low-density lipoprotein receptor-related protein 8 (LRP8) are required for the exercise-induced increase in adult hippocampal neurogenesis. In vivo selenium infusion increased hippocampal neural precursor cell (NPC) proliferation and adult neurogenesis. Mimicking the effect of exercise through dietary selenium supplementation restored neurogenesis and reversed the cognitive decline associated with aging and hippocampal injury, suggesting potential therapeutic relevance. These results provide a molecular mechanism linking exercise-induced changes in the systemic environment to the activation of quiescent hippocampal NPCs and their subsequent recruitment into the neurogenic trajectory.
Keyword(s): Aging (MeSH) ; Animals (MeSH) ; Cell Proliferation (MeSH) ; Hippocampus (MeSH) ; Mice (MeSH) ; Neural Stem Cells: metabolism (MeSH) ; Neurogenesis: physiology (MeSH) ; Selenium: metabolism (MeSH) ; Selenium: pharmacology (MeSH) ; adult neurogenesis ; aging ; dentate gyrus ; endothelin-1 ; exercise ; hippocampal lesion ; hippocampus ; neural precursor cell ; neural stem cell ; selenium
![]() |
The record appears in these collections: |