Yesterday afternoon, on the 8th day of the Winter Olympics, China won the fourth golden ice pier! Gao Tingyu won the gold medal in the men's 500m speed skating and broke the Olympic record with a time of 34.32 seconds!
With the enthusiastic holding of the Winter Olympic Games, the concept of "life lies in sports" has once again been deeply rooted in the hearts of the people. Sports, as a very low-cost means of maintaining physical health, has long been popularized with the phenomenon of "night running and punching cards", "square dance", "everyone lifting iron" and so on.
So, are the "benefits" of exercise limited to physical health? Not! The benefits of luck don't stop there – sports-loving people may be smarter than others!
In recent years, scientists have discovered that exercise promotes brain development, and numerous experimental results have shown that exercise causes nerves in the hippocampus region of the brain to generate or create new neurons, and the hippocampus plays a vital role in learning, memory and mood regulation. So the question is, how does exercise promote neuronal occurrence?
Back in the 1990s, researchers in the United States made groundbreaking discoveries: mice's roller movements increased the hippocampal neurons in their brains, a process linked to the production of a protein called brain-derived neurotrophic factor (BDNF).
When the researchers "sprinkled" BDNF on the nerve cells inside the dish, the cells spontaneously formed new branches. The more BDNF is secreted, the stronger the connections between neurons, and the more and stronger the brain synapses are likely to weave more and stronger neural networks, making our brains stronger.
BDNF performs synaptic plasticity through a variety of mechanisms. (Image source: ResearchGate.com)
In the decades that followed, different activation pathways of exercise-boosted brain neurons were discovered, including histase B, platelet factor 4, and vascular endothelial growth factor, but BDNF was still considered to be the most effective. At the beginning of the new year, however, its "hegemonic" status was challenged.
Recently, the article published in Cell Metabolism by a joint multi-team of mainland scholars Hou Shengtao/Zhuo Zhan once again provides new insights into the question of how exercise promotes neurogenesis.
The authors believe that selenium-containing proteins produced during exercise are the key to helping the brain grow new neurons, and humans may be able to use dietary supplements with selenium to reverse cognitive decline due to aging and brain damage.
(Image source: Cell Metabolism)
This conclusion stemmed from a study by the authors' team several years ago, when researchers screened mice that did roller motion for 4 days and mice that did not exercise separately, and determined that 68 protein levels increased after exercise.
One of these proteins, called selenoprotein P (SEPP1), has particularly caught everyone's attention – SEPP1 can transport selenium to the brain, and its content has more than tripled after rodent exercise!
Since the seppp1 protein content of the exercised mice has changed significantly, is selenium a key factor in post-exercise neurogenesis? What is its mechanism? The researchers decided to conduct a more in-depth study.
Selenium is a trace element rich in nuts, purple potatoes and other foods, and is inexpensive and easy to obtain. In the latest study, they chose to add two exogenous forms of selenium — sodium selenite (in the form of salt in water and soil) or selenomethionine (present in the form of amino acids in the diet) — into neural precursor cells (NPCs, which produce new neurons).
Surprisingly, in just 14 days, the number of these "neural precursor cells" doubled! When the researchers injected sodium selenite directly into the brains of mice for 7 days, the number of neural precursor cells in the hippocampus also tripled!
Selenium injection increases the number of proliferating precursor cells in mouse DGs, but has no effect on the number of proliferating cells in SVZ
LRP8 is the receptor of SEPP1 on cerebral capillary endothelial cells, and when the two are combined, selenium transport can be transported through the blood-brain barrier into the brain and play an effective role. From this, the researchers constructed mice lacking SEPP1 or its receptors, and found that when the Sepp1 or Lrp8 gene was knocked out, the neural precursor cells of mice that had been in motion for 7 days did not increase, which further confirmed that SEPP1 is the key to motor manufacturing new neurons.
Exercise-induced increase in NPC proliferation requires Sepp1-Lrp8-mediated selenium transport
Juan Encinas, a neurobiologist at the Achucarro Basque Neuroscience Centre, commented: "This is the first time that substances commonly present in the diet have such a pronounced effect on neurogenesis. ”
So, if selenium is supplemented in the daily diet, can it improve brain aging?
Therefore, the researchers "incidentally" tested the brain cognition of mice. The team added selenomethionine to the drinking water of 18-month-old mice (the equivalent of a 60-year-old human) — and nearly 1 month later, the number of new neurons in the rodent hippocampus doubled!
The delivery of dietary selenium-L-methionine leads to a significant increase in the number of proliferating precursor cells (D and F) and immature neurons (E) in the DG
Mice in the selenium treatment group also performed superiorly in two memory tasks that relied on the hippocampus region. In active avoidance experiments, mice treated with selenium were significantly better than control mice at avoiding shock zones and received fewer shocks; in the maze experiment, mice treated with selenium also learned to enter the escape box faster than control mice.
Finally, the researchers investigated whether selenium could help reverse cognitive deficits caused by brain damage. They injected the vasoconstrictor ET-1 molecule into the hippocampus of mice to cause stroke-like lesions that disrupt neurons and impair memory. In a range of memory tasks, the damaged but selenium-treated mice performed as well as normal mice. Untreated damaged mice, on the other hand, were unable to recognize objects as new, and they had a hard time remembering where they had received an electric shock the day before.
Selenium rescues hippocampal learning and memory impairment caused by endothelin-induced hippocampal damage
Speaking of which, it's really a "remarkable" study — not only revealing the mechanism by which exercise promotes neurogenesis and improves cognitive function in adulthood, but also developing new uses for selenium, a "favorite" element in food. This is undoubtedly good news for people who cannot exercise due to physical reasons such as advanced age or weakness.
Finally, remind everyone who is overusing your brain: exercise hard, eat more selenium-rich foods such as nuts, grains and dairy products, and a smart brain is "beckoning" to you.
Resources:
[1] Self-amplifying autocrine actions of BDNF in axon development. Proc Natl Acad Sci U S A. 2011 Nov 8;108(45):18430-5. doi: 10.1073/pnas.1115907108.
[2] Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits induced by hippocampal injury and aging. Cell Metab. 2022 Jan 31:S1550-4131(22)00005-5. doi: 10.1016/j.cmet.2022.01.005.
Written by | Happy one
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