Scientists have made a groundbreaking discovery about the adult brain’s ability to repair itself after injury or certain autoimmune diseases. A study conducted by researchers at the University of Zurich has found that the adult brain has a remarkable hidden repair system that allows it to rebuild damaged cellular networks.

The researchers discovered that specialized support cells called astrocytes play a crucial role in this repair process. Astrocytes are responsible for providing nerve cells with nutrients, controlling blood flow, and supporting the overall health of brain tissue. In the past, scientists believed that once astrocytes were destroyed, the adult brain could not fully replace them.

However, the new study challenges this long-standing view. The research team, led by co-lead authors Marina Herwerth and Matthias Wyss, identified a specialized population of ‘regenerative’ astrocytes in the brains of living mice. These cells gather around the edges of damaged brain regions and help rebuild the lost astrocyte network.

The researchers used two-photon microscopy to observe the brains of living mice in real-time for several weeks. They also tracked which genes became active in different regions of the brain. Together, these methods allowed the team to identify the astrocytes responsible for restoring injured tissue.

The regenerative cells do more than simply divide. They also carry out an unusual process in which newly created nuclei from daughter cells travel considerable distances through the astrocytes toward the damaged region. As Bruno Weber, one of the study’s authors, explains, ‘they send the newly formed nuclei of their daughter cells gliding across long distances to repopulate the damaged area of the brain and knit the astrocyte network back together.’

The finding that cell nuclei can move through the long extensions of adult astrocytes into injured tissue adds a new dimension to scientists’ understanding of how the brain organizes its own repair after certain types of damage. If researchers eventually learn how to selectively activate these repair mechanisms, they may be able to promote more effective restoration of damaged brain tissue, rebuild astrocyte networks, and improve recovery from certain brain disorders.

The team also identified many genes and signaling pathways that become temporarily active while the repair process is underway. These biological signals may provide potential targets for future efforts to influence regeneration after disease or injury. As Bruno Weber stresses, ‘we were able to identify numerous genes and signaling pathways that are temporarily activated during repair. They could serve as starting points in the future for influencing post-disease and -injury regeneration processes.’