Feb 17, 2026
3 min read
Our brain ages along with the rest of our body, and as it ages, it produces fewer brain cells.
Our brains age along with the rest of our bodies, and as they do, they produce fewer new brain cells.Now researchers have identified a key mechanism that slows the age-related decline in neuron production.
In later life, the neural stem cells (NSCs) that turn into full-fledged neurons become more dormant - almost as if they retire after a long life.When this happens, cognitive decline sets in.
The main reason NSC activity declines with age is the wear and tear of telomeres, the protective caps at the ends of DNA.Telomeres break down a little more each time a cell divides, and over time this impairs the cells' ability to grow and divide, leading to increased cell death.
This latest study, led by a team from the National University of Singapore (NUS), looked closely at the methods involved to see if they could find a way to regenerate weakened NSCs.
Biochemist Derrick Sek Tong Ong, from NUS, said:
"A lack of neural stem cell regeneration prevents the formation of new cells needed to support learning and memory functions."
"Although studies have shown that regeneration of defective neural stem cells can be partially restored, the underlying mechanisms are still poorly understood."
By analyzing human NSC in the laboratory and in mouse model experiments, the researchers identified a protein called cyclin D-binding Myp-like transcription factor 1 (DMTF1).Transcription factors such as DMTF1 bind to DNA, turning genes on or off.
DMTF1 is not new, but its role in influencing NSCs is.The team found it was more common in young, healthy people, and adding more DMTF1 encouraged NSCs to grow and divide – potentially restoring the production of natural neuron cells associated with the young brain.
While shorter telomeres appear to contribute to reduced DMTF1 levels, when the amount of DMTF1 is artificially increased in cells, telomere length remains unchanged—so the transcription factor appears to have found a solution.
In particular, DMTF1 activates two “helper” genes called Arid2 and Ss18, which promote cell growth by altering genes that restart the biological cycle by which neurons are produced.
Understanding this process at such a fundamental level means that we will eventually be able to control it, perhaps through treatments that stimulate neuronal growth regardless of age.
"Our results show that DMTF1 contributes to the proliferation of neural stem cells in neuroaging," says neuroscientist Liang Yajing from NUS.
This is an important discovery of an important process, but we should not get ahead of ourselves: this study is based on laboratory experiments and mouse models, and any suggestion that it is possible to increase the production of neurons has yet to be proven.
However, now that this mechanism has been identified, future studies can build on this research.It's possible that changing DMTF1 could reverse some of the aging that normally affects the brain, but that remains to be seen.
Next steps may include a broader analysis of how DMTF1 can be used to restore NSC function and whether it improves learning and memory.In animal studies this should first be done carefully;DMTF1 is associated with cell growth, so overexpression can lead to cancerous tumors.
We can add this latest study to a growing body of research on how our brain ages and how some aging processes can be slowed, stopped or reversed.
Diet and exercise seem to help, but the lure of treatments to rejuvenate aging brain cells remains strong, albeit a distant prospect.
Related: Stress-sensitive neurons can have powerful effects on our entire brain
The aging brain is vulnerable to cognitive problems, disease, and dementia.Although this research doesn't directly address the problem, it goes some way to helping us understand the aging brain.
"Understanding the mechanisms of neural stem cell regeneration provides a powerful basis for studying age-related cognitive decline," says Ong.
The research was published in the journal Science Advances.
