Summary: Research from the University of Queensland indicates that selenium, a dietary trace mineral found in foods like grains, meat and nuts, can restore learning and memory after hippocampal injury and improve neurogenesis and cognition in aging brains.
Source: University of Queensland
Key finding: Selenium — a naturally occurring mineral present in many common foods — may help reverse cognitive decline following stroke-like hippocampal injury and support learning and memory in older brains, according to research led by the Queensland Brain Institute.
Dr. Tara Walker and colleagues observed that physical exercise increased levels of a blood-borne selenium transport protein, and this prompted investigation into whether dietary selenium could reproduce some of exercise’s positive effects on the aging brain.
For decades, scientists have known that regular physical activity promotes the creation of new neurons in the adult brain, particularly within the hippocampus, a region central to learning and memory. What remained unclear were the systemic molecular signals that mediate this response.
The research team used animal models to explore whether selenium supplementation could mimic the neurogenic and cognitive benefits of exercise. They found that supplying selenium increased the production of new neurons and improved performance on learning and memory tasks in aged mice.
In aging animals — and in humans — the rate of new neuron formation in the hippocampus declines markedly. In the study, mice receiving selenium supplements showed a recovery in neurogenesis that corresponded with improved cognitive function, effectively reversing some age-related deficits.
Selenium is an essential trace element absorbed from soil and water and incorporated into food chains. It is present in a range of dietary sources including grains, meat and nuts, with particularly high concentrations reported in Brazil nuts.
The team also tested whether selenium could affect cognitive impairments that follow hippocampal injury, a condition that models some effects of stroke. Young mice that normally perform well on learning and memory tests lost that ability after hippocampal injury, but treated animals regained cognitive performance when given selenium.
These findings point to a potential therapeutic route for enhancing cognition in people who cannot exercise due to frailty, illness or advanced age. However, researchers emphasize that selenium supplements are not a full replacement for the broad health benefits of physical activity.
Dr. Walker cautioned that while a balanced diet typically provides adequate selenium for most people, supplementation might benefit older adults or individuals with neurological conditions under medical supervision. Excessive selenium intake can be harmful, so any consideration of supplements should involve healthcare advice.
About this memory research news
Author: Press Office
Source: University of Queensland
Contact: Press Office – University of Queensland
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Original Research: Open access. “Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits induced by hippocampal injury and aging” by Odette Leiter et al., published in Cell Metabolism.
Abstract (summary)
Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits induced by hippocampal injury and aging
Although the ability of exercise to enhance neurogenesis has been well described, the molecular pathways that link systemic changes from exercise to activation of neural precursor cells were not fully understood. This study identifies a selenium transport protein, selenoprotein P (SEPP1), as a systemic mediator released in response to exercise.
Using genetic knockout mouse models, the researchers showed that SEPP1 and its receptor, low-density lipoprotein receptor-related protein 8 (LRP8), are required for exercise-driven increases in adult hippocampal neurogenesis. Experimental infusion of selenium in vivo boosted proliferation of hippocampal neural precursor cells and increased adult neurogenesis.
Importantly, dietary selenium supplementation produced effects that mimicked exercise: it restored neurogenesis and reversed cognitive decline associated with both aging and hippocampal injury in the models tested. These results offer a molecular link between exercise-induced systemic changes and recruitment of quiescent hippocampal precursor cells into active neurogenic pathways, highlighting potential therapeutic relevance while underscoring the need for careful evaluation of dosage and safety in clinical contexts.