Iranian researchers at the University of Tehran have identified molecular changes that may help explain why the brain gradually loses its ability to repair itself in people with Alzheimer’s disease, opening new avenues for future treatments.
The findings could provide a new direction for developing future treatments aimed not only at protecting existing brain cells but also at restoring the brain’s natural capacity to produce new neurons.
The research was conducted by scientists at the Institute of Biochemistry and Biophysics at the University of Tehran, using single-cell RNA sequencing technology to investigate changes in gene activity associated with impaired neurogenesis — the process through which new neurons are formed in the brain.
Unlike conventional approaches that examine groups of cells together, this technology allows researchers to study gene activity in individual cells, offering a more detailed picture of how different types of brain cells respond to Alzheimer’s disease.
Professor Bahram Gliaei, who led the research team, said Alzheimer’s should not be understood simply as a disease that causes neurons to die, it also affects the brain’s ability to repair itself.
“The study found reduced activity in genes responsible for maintaining neural stem cells and supporting their normal development into neurons,” he said.
Neural stem cells are important because they can develop into new nerve cells, potentially helping the brain maintain and repair its networks.
However, according to Gliaei, their findings suggest that in Alzheimer’s-affected samples, these cells are more likely to develop into astrocytes — support cells that help maintain the brain’s environment — rather than becoming new neurons.
At the same time, he added, the activity of certain genes involved in maintaining the population of neural stem cells was also reduced.
“This could contribute to a decline in the number of these cells and further limit the brain’s ability to generate new neurons,” he highlighted.
The researchers believe these changes may be linked to the gradual deterioration of neural networks in the hippocampus, a brain region essential for learning and memory.
The findings highlight a potentially important aspect of Alzheimer’s that goes beyond the loss of existing brain cells: the disruption of the brain’s natural regeneration mechanisms.
Understanding these molecular processes could help scientists explore treatments that target the restoration of neurogenesis, rather than focusing exclusively on preventing neuronal damage.


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