> Most neurons in the human brain last a lifetime, and for good reason. Intricate, long-term information is preserved in the complex structural relationships between their synapses. To lose the neurons would be to lose that critical information — that is, to forget.
> Intriguingly, some new neurons are still produced in the adult brain by a population of cells called neural stem cells. As brains age, however, they become less and less adept at making these new neurons, a trend that can have devastating neurological consequences, not just for memory, but also for degenerative brain diseases such as Alzheimer’s and Parkinson’s and for recovery from stroke or other brain injury.
> A new Stanford Medicine study, published Oct. 2 in Nature, sheds hopeful new light on how and why neural stem cells, the cells behind the generation of new neurons in the adult brain, become less active as brains age. The research also suggests some intriguing next steps in addressing old neural stem cell passivity — or even stimulating neurogenesis, the production on new neurons, in younger brains in need of repair — by targeting newly identified pathways that could reactivate the stem cells.
> “We first found 300 genes that had this ability — which is a lot,” emphasized Brunet, the Michele and Timothy Barakett Endowed Professor. After narrowing the candidates down to 10, “One in particular caught our attention,” Brunet said. “It was the gene for the glucose transporter known as the GLUT4 protein, suggesting that **elevated glucose levels** in and around old neural stem cells could be keeping those cells inactive.”
> The glucose transporter connection “is a hopeful finding,” Brunet said. For one, it suggests not only the possibility of designing pharmaceutical or genetic therapies to turn on new neuron growth in old or injured brains, but also the possibility of developing simpler behavioral interventions, such as a low carbohydrate diet that might adjust the amount of glucose taken up by old neural stem cells.
> “The next step,” Brunet continued, “is to look more closely at what glucose restriction, as opposed to knocking out genes for glucose transport, does in living animals.”
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> Most neurons in the human brain last a lifetime, and for good reason. Intricate, long-term information is preserved in the complex structural relationships between their synapses. To lose the neurons would be to lose that critical information — that is, to forget.
> Intriguingly, some new neurons are still produced in the adult brain by a population of cells called neural stem cells. As brains age, however, they become less and less adept at making these new neurons, a trend that can have devastating neurological consequences, not just for memory, but also for degenerative brain diseases such as Alzheimer’s and Parkinson’s and for recovery from stroke or other brain injury.
> A new Stanford Medicine study, published Oct. 2 in Nature, sheds hopeful new light on how and why neural stem cells, the cells behind the generation of new neurons in the adult brain, become less active as brains age. The research also suggests some intriguing next steps in addressing old neural stem cell passivity — or even stimulating neurogenesis, the production on new neurons, in younger brains in need of repair — by targeting newly identified pathways that could reactivate the stem cells.
> “We first found 300 genes that had this ability — which is a lot,” emphasized Brunet, the Michele and Timothy Barakett Endowed Professor. After narrowing the candidates down to 10, “One in particular caught our attention,” Brunet said. “It was the gene for the glucose transporter known as the GLUT4 protein, suggesting that **elevated glucose levels** in and around old neural stem cells could be keeping those cells inactive.”
> The glucose transporter connection “is a hopeful finding,” Brunet said. For one, it suggests not only the possibility of designing pharmaceutical or genetic therapies to turn on new neuron growth in old or injured brains, but also the possibility of developing simpler behavioral interventions, such as a low carbohydrate diet that might adjust the amount of glucose taken up by old neural stem cells.
> “The next step,” Brunet continued, “is to look more closely at what glucose restriction, as opposed to knocking out genes for glucose transport, does in living animals.”