Study Finds Human Protein Linked to Reversing Brain Aging - Video

Aging often brings a gradual decline in memory and learning ability, largely because neural stem cells lose their capacity to produce new neurons. For decades, this slowdown has been viewed as an unavoidable consequence of growing older. However, researchers at the National University of Singapore (NUS) have uncovered evidence suggesting this process may not be entirely irreversible.

In a study published in Science Advances, the team identified a key protein called cyclin D-binding myb-like transcription factor 1 (DMTF1) as a central regulator of neural stem cell function. Transcription factors like DMTF1 control how genes are switched on or off. When scientists examined aged human and mouse neural stem cells, they found that DMTF1 was present but largely silenced, leaving the cells unable to regenerate effectively.

When researchers restored DMTF1 activity in these aged stem cells, the results were striking. The cells regained their ability to proliferate, essentially reviving their regenerative potential. According to senior author Derrick Sek Tong Ong, this finding sheds light on mechanisms that have long been poorly understood in brain aging.

The team also investigated how DMTF1 overcomes one of aging’s most well-known barriers: telomere shortening. Telomeres, protective caps at the ends of chromosomes, naturally shrink as cells divide, eventually triggering cellular senescence. Yet DMTF1 appeared to bypass this limitation by activating growth-related genes through chromatin remodeling, even in cells already affected by shortened telomeres.

While the research was conducted in laboratory models rather than living humans, it provides a promising framework for future therapies. Instead of reversing aging, targeting DMTF1 could potentially help the brain maintain its ability to repair and regenerate neurons, preserving cognitive function later in life.

REFERENCE: Yajing Liang, Oleg V. Grinchuk, et al.; DMTF1 up-regulation rescues proliferation defect of telomere dysfunctional neural stem cells via the SWI/SNF-E2F axis; Science Advances; DOI: 10.1126/sciadv.ady5905