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SAN DIEGO (CNS) – Injured adult brain cells revert to an embryonic state and become capable of re-growing new connections, which under the right conditions can help restore lost brain function, according to findings published Wednesday by researchers at UC San Diego School of Medicine.

The findings, published in the academic journal ‘Nature,’ were part of a collaborative study between UC San Diego, UCLA and the University of Tennessee.

Repairing damage to the brain and spinal cord, until relatively recently, seemed an impossible task. The new study lays out a “transcriptional roadmap of regeneration in the adult brain.”

“Using the incredible tools of modern neuroscience, molecular genetics, virology and computational power, we were able for the first time to identify how the entire set of genes in an adult brain cell resets itself in order to regenerate,” said senior author Dr. Mark Tuszynski, professor of neuroscience and director of the Translational Neuroscience Institute at UC San Diego School of Medicine. “This gives us fundamental insight into how, at a transcriptional level, regeneration happens.”

Using a mouse model, Tuszynski and colleagues discovered that after injury, mature neurons in adult brains revert back to an embryonic state.

“Who would have thought,” Tuszynski said. “Only 20 years ago, we were thinking of the adult brain as static, terminally differentiated, fully established and immutable.”

To provide an “encouraging environment for regrowth,” Tuszynski and colleagues investigated how damaged neurons respond after a spinal cord injury. In recent years, researchers have significantly advanced the possibility of using stem cells to spur spinal cord injury repairs and restore lost function, essentially by inducing neurons to extend nerve fibers through and across an injury site, reconnecting severed nerves.

The latest study produced a second surprise: In promoting neuronal growth and repair, one of the essential genetic pathways involves the gene Huntingtin, which, when mutated, causes Huntington*s disease, a devastating disorder characterized by the progressive breakdown of nerve cells in the brain.

“While a lot of work has been done on trying to understand why Huntingtin mutations cause disease, far less is understood about the normal role of Huntingtin,” Tuszynski said. “Our work shows that Huntingtin is essential for promoting repair of brain neurons. Thus, mutations in this gene would be predicted to result in a loss of the adult neuron to repair itself. This, in turn, might result in the slow neuronal degeneration that results in Huntington’s disease.”