Scientists found protein could keep aged neural stem cells active by restoring DMTF1, reviving their regenerative capacity and offering a potential path to slow age-related cognitive decline.
Study Links DMTF1 Loss To Stem Cell Aging
Scientists found protein could keep the brain from age-related decline, as researchers from the National University of Singapore identified DMTF1’s role in counteracting neural deterioration.
In a study published in Science Advances, the team reports that cyclin D-binding myb-like transcription factor 1, or DMTF1, is repressed in aged neural stem cells. When the protein’s expression is restored, the cells regain their ability to proliferate.
As the brain ages, neural stem cells regenerate less efficiently. That decline contributes to reduced learning and memory and is linked to broader cognitive impairment.
“While previous studies have found that defective neural stem cell regeneration can be partially restored, its underlying mechanisms remain poorly understood,” said Derrick Sek Tong Ong, the study’s senior author, in a statement. “Understanding the mechanisms for neural stem cell regeneration provides a stronger foundation for studying age-related cognitive decline.”
Experiments Show Regeneration Without Telomere Repair
The research team used human stem cell systems and mouse models to simulate aging. They then conducted transcriptome analyses and genome-binding studies to examine how DMTF1 regulates gene activity.
Aging cells typically show shortened telomeres, protective DNA sequences at the ends of chromosomes. As telomeres shrink over time, cells can enter senescence, reducing division and increasing inflammation.
The researchers found that DMTF1 regulates helper genes that activate growth-related genes through chromatin remodeling, a process that alters how DNA is packaged and expressed.
Scientists found protein could keep neural stem cells proliferating even when telomeres shorten, as restoring DMTF1 reactivated dormant regenerative pathways despite ongoing cellular aging.
The findings indicate that targeting DMTF1 could help reverse age-related decline in neural stem cells by restarting the molecular machinery responsible for cell division.
Findings Offer Framework For Future Therapies
The study’s authors caution that the experiments were conducted outside the human body. Further research is required before potential therapies can be tested in people.
“Our findings suggest that DMTF1 can contribute to neural stem cell multiplication in neurological aging,” said Liang Yajing, a co-author of the study. “While our study is in its infancy, the findings provide a framework for understanding how aging-associated molecular changes affect neural stem cell behavior, and may ultimately guide the development of successful therapeutics.”
Scientists say the work does not amount to reversing aging. Instead, it focuses on preserving regenerative function in the brain as organisms grow older.
If future studies confirm the results in humans, therapies targeting DMTF1 could help mitigate some of the most serious cognitive effects associated with aging, including memory loss and reduced learning capacity.
For now, researchers say the discovery advances understanding of how molecular changes drive neural stem cell decline and opens new avenues for studying age-related brain disorders.
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