In only we could replace the neurons in our brains, we could basically have a the elastic mind of a child forever. Indeed, if we could replace neurons, we would be able to reverse those neural deficits associated with and/or caused by brain injury, stroke, or even Alzheimer’s disease.
But unfortunately, we cannot replace neurons; at least not right now. Maybe in time we will learn how. Until then, though, maybe we can encourage the brain to regrow them. Or, rather, maybe we can reprogram the body to use other cells as replacement neurons.
This is what a team of researchers are investigating at present, and they have published their latest findings in the journal Stem Cell Reports. In the report, researchers indicate that it may be possible to reprogram astrocytes to become neurons. Since they only form and proliferate after a brain injury, reprogramming these cells to become neurons is almost like growing brand new ones, essentially.
Now, that sounds simple enough in theory, but it is not an easy feat. Gene therapy is one potential method, but it requires that the new gene be delivered into the body along with viral particles. Of course, gene therapy also costs about $500,000 per patient (for a single administration).
Chemical conversion is another possibility but, simply, it can be clinically difficult because its complexity can require a more advanced laboratory.
But the Penn State research team developed a simpler chemical conversion cocktail that they hope can be delivered more efficiently.
In an article titled “Chemical Conversion of Human Fetal Astrocytes into Neurons through Modulation of Multiple Signaling Pathways,” the study authors explain the discovery. The write: “We demonstrate that modulation of three to four signaling pathways among Notch, glycogen synthase kinase 3, transforming growth factor beta, and bone morphogenetic protein pathways is sufficient to change an astrocyte into a neuron. The chemically converted human neurons can survive more than 7 months in culture, fire, repetitive action potentials, and display robust synaptic burst activities.”
Essentially, the article describes how they managed to reduce the number of molecules involved to just a few as a means to simplify administration. Furthermore, the article indicates that they achieved at least some success with early testing. The key now, then, Is to continue testing with different formulas to observe efficacy and, of course, risk, but also to assess accessibility in a clinical setting.