The adult brain repairs itself by reverting to embryonic state

The adult brain repairs itself by reverting to embryonic state

When adult brain cells are injured, they revert to an embryonic state, according to new findings published in the journal Nature. The scientists report that in their newly adopted immature state, the cells become capable of re-growing new connections that, under the right conditions, can help to restore lost function.

Repairing damage to the brain and spinal cord may be medical science's most daunting challenge. Until relatively recently, it 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. This gives us fundamental insight into how, at a transcriptional level, regeneration happens," said senior author.

Using a mouse model, the authors discovered that after injury, mature neurons in adult brains revert back to an embryonic state. "Who would have thought," said the senior author. " To provide an "encouraging environment for regrowth," the authors investigated how damaged neurons respond after a spinal cord injury.

In recent years, researchers have significantly advanced the possibility of using grafted neural stem cells to spur spinal cord injury repairs and restore lost function, essentially by inducing neurons to extend axons through and across an injury site, reconnecting severed nerves.

Last year, for example, a multi-disciplinary team described using 3D printed implants to promote nerve cell growth in spinal cord injuries in rats, restoring connections and lost functions.

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

The team found that the "regenerative transcriptome" -- the collection of messenger RNA molecules used by corticospinal neurons -- is sustained by the HTT gene. In mice genetically engineered to lack the HTT gene, spinal cord injuries showed significantly less neuronal sprouting and regeneration.

"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," the senior author 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."