Deep in your brain, neural stem cells that once produced fresh neurons have essentially retired. By your 60s, the factory that builds new brain cells has practically shut down. But a team at the National University of Singapore just found the protein responsible for that shutdown — and when they restored it, those retired stem cells went right back to work.
The study, published February 12th in Science Advances, identifies a protein called DMTF1 (cyclin D-binding myb-like transcription factor 1) as the key molecular switch. Led by Dr. Liang Yajing under Assistant Professor Derrick Sek Tong Ong, the research maps the entire chain reaction behind age-related neural stem cell dormancy.
Here’s how it works: as we age, the telomeres — protective caps on the ends of our chromosomes — get shorter with each cell division. Eventually they get so short that cells stop dividing. The Singapore team discovered that this telomere shortening specifically depletes DMTF1 levels. Without DMTF1, two helper genes called Arid2 and Ss18 go quiet. These genes are part of the SWI/SNF chromatin remodeling complex, which normally loosens tightly packed DNA to expose growth-related genes. When they’re inactive, growth genes stay silenced and stem cells remain dormant.
The breakthrough: when researchers artificially restored DMTF1 in aged stem cells, the cells started dividing again — even though the telomeres remained short. DMTF1 essentially overrides the retirement notice, bypassing the consequences of telomere aging without reversing the aging itself.
This is still early-stage research done in cell cultures and mouse models. The next steps involve testing whether boosting DMTF1 can improve learning and memory in living animals without increasing brain tumor risk. Professor Ong described the work as “in its infancy.”
But the implications are profound. If a single protein can reawaken dormant neural stem cells, future therapies might target DMTF1 to combat Alzheimer’s, age-related cognitive decline, and other neurodegenerative conditions. The brain’s repair machinery isn’t broken — it’s just been switched off. And now we may know which switch to flip.