Journal
CELL METABOLISM
Volume 34, Issue 3, Pages 408-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2022.01.005
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Funding
- Brazil Family Foundation for Neurology, Australia
- Deutsche Forschungsgemeinschaft [SFB 655]
- Clem Jones Centre for Ageing Dementia Research
- SUSTech-UQ Joint Graduate Student Scholarship
- National Natural Science Foundation of China [81871026]
- Shenzhen-Hong Kong Institute of Brain Science-Shenzhen Fundamental Research Institutions [2019SHIBS0002, 2021SHIBS0002]
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Exercise enhances adult hippocampal neurogenesis through the systemic release of the antioxidant selenium transport protein, SEPP1, providing a potential therapeutic approach for cognitive decline associated with hippocampal injury and aging.
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.
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