Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits induced by hippocampal injury and aging

Lots more work to get done here.  Human research needed. WHOM will be doing that? What is the delivery system needed for selenium? What is the amount per bodyweight and sex? 

Of course nothing was done with this earlier selenium research. Heads need to roll for such cesspools of incompetence.

• selenium (3 posts to May 2015)

Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits induced by hippocampal injury and aging

Author links open overlay panelOdetteLeiter¹²³⁸ZhanZhuo¹⁴⁸RuslanRust²³¹⁰Joanna M.Wasielewska²³LisaGrönnert²³¹¹SusannKowal²³Rupert W.Overall²³Vijay S.Adusumilli²³Daniel G.Blackmore¹AdamSouthon⁵KatherineGanio⁶Christopher A.McDevitt⁶NicoleRund²³DavidBrici¹Imesh AththanayakeMudiyan¹Alexander M.Sykes⁷Annette E.Rünker²³SaraZocher²³…Tara L.Walker¹²³⁹¹²

https://doi.org/10.1016/j.cmet.2022.01.005Get rights and content

Under a Creative Commons license

Open access

Highlights

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Selenium mediates the exercise-induced increase in adult hippocampal neurogenesis

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Selenium increases hippocampal precursor proliferation and adult neurogenesis

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Selenium reverses cognitive decline in aging and in hippocampal injury

Summary

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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