US researchers find that certain nerve cells that have the ability to regrow are needed for axon regeneration, providing hope for conditions such as blindness and paralysis.


Researchers at the University of Connecticut (UConn) School of Medicine in the United States have made a significant discovery that could potentially restore vision and movement to people suffering from nerve damage. The results, published in the journal Developmentreveal the existence of a small population of nerve cells in all who have the ability to regrow, offering new hope for conditions such as glaucoma, optic neuritis and paralysis.

Blindness and paralysis affect millions of people worldwide, with glaucoma alone affecting over 3 million people in the United States. While these conditions may seem distinct, they share a common underlying cause: the inability of adult nerve cells to regenerate their connections, known as axons.

While some animals possess the remarkable ability to regrow axons, mammals such as mice and humans have not demonstrated this ability. Scientists previously believed that the immature nerve cells needed for axon regeneration were absent in mammals.

However, researchers at the UConn School of Medicine, led by neuroscientist Ephraim Trakhtenberg, have discovered a population of neurons that behave similarly to embryonic nerve cells. These neurons express a specific subset of genes and can be experimentally stimulated to regrow axons over long distances, potentially leading to the restoration of vision and mobility. They identified two genes, associated with mitochondria Dynlt1a AND Lars2that were upregulated during axon regeneration, presenting novel therapeutic targets for gene therapy.

Trakhtenberg believes similar immature nerve cells may exist in other brain regions besides the visual system, pointing to the possibility of treating paralysis as well. However, creating the optimal conditions for axon regeneration presents a significant challenge. While these embryonic nerve cells can regrow axons in response to certain treatments, the axons often become blocked before they reach their intended targets.

Previous research has shown that factors such as cell maturity, gene activity, signaling molecules within axons, as well as scarring and inflammation at the site of injury inhibit axon regeneration. While some therapies targeting genes, signaling molecules, and the environment of the injury site have shown promise in promoting limited axon growth, they often fail to achieve the necessary length.

Typically, axons in embryos grow to their full length before being coated in myelin, but the team found that the cells that apply myelin start interacting with the regenerating axons shortly after they start growing. This interaction, which precedes the isolation process, contributes to stalling the axons so they never reach their targets.

The researchers suggest that a multi-pronged approach would be needed to fully regenerate injured axons. Therapies targeting both the gene and the signaling activity within the nerve cells would be needed to encourage them to grow as an embryonic nerve cell would. By clearing the environment of inhibitory molecules and disrupting oligodendrocyte isolation, axons would have time to reconnect with their targets in the central nervous system before being myelinated. Thus, treatments that encourage oligodendrocytes to myelinate axons would complete the healing process.

Although in some types of complex lesions the protection by myelination of still intact but demyelinated axons from subsequent inflammatory damage may take precedence, ultimately the secondary inflammatory damage can be controlled pharmacologically, paving the way for suspension of myelination and uncontrolled therapeutic regeneration of axons. axons for these types of injuries like well, Trakhtenberg explained.

New insights into how axons grow could one day create a pathway for truly effective therapies for blindness, paralysis and other ailments caused by nerve damage.

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