Scientists have found a way to speed up the recovery of damaged nerves

Damaged nerves in adult mammals do not recover well, which is why injuries to the peripheral nerves and spinal cord can lead to prolonged or permanent movement and sensitivity disorders. Researchers from the Icahn School of Medicine at Mount Sinai have discovered a protein that, according to their data, acts as a kind of "brake" for the repair of nerve fibers. In experiments on mice, blocking this protein helped damaged nerves to grow outgrowths more actively and improved the restoration of movement and sensitivity. How the body reacts to nerve damage and why the mechanism found can help speed up their recovery is in the Izvestia material.

Protein prevents damaged nerves from repairing

The researchers drew attention to the AHR protein, the aryl carbohydrate receptor, which is involved in the reaction of cells to various environmental substances. Scientists have discovered that after nerve damage, AHR suppresses the growth of axons, the long outgrowths of nerve cells through which signals are transmitted.

When the researchers removed AHR from neurons or blocked its activity with drugs, the damaged nerve fibers recovered more successfully. In experiments on mice, AHR suppression also helped improve movement and sensitivity after damage to peripheral nerves and spinal cord.

The results of the work are published in the journal Nature. Researchers believe that AHR may be an important regulator of how nerve cells allocate resources after injury.

Scientists have discovered a hidden mechanism for repairing brain cells

Neurons choose between survival and recovery after injury

Scientists have found that AHR performs a kind of protective function. After damage, the nerve cell faces severe stress and must maintain the normal state of the proteins inside itself. This process is called proteostasis and helps the neuron survive the effects of injury.

However, this protective reaction simultaneously limits the production of new proteins needed to repair the damaged axon. Therefore, the neuron is faced with a peculiar biological choice: first to maintain its own condition and survive stress, or to direct more resources to the restoration of the neural process.

When the AHR was blocked, the cells changed their priority. They began to produce proteins more actively and turned on biological mechanisms related to the growth and regeneration of axons. Experiments have shown that another protein, HIF—1a, is involved in this process, which regulates the work of genes related to metabolism and tissue repair.

Thus, the problem may lie not only in the fact that adult nerve cells are poorly able to repair damaged appendages. After an injury, they also receive a signal to focus on their own survival, and the AHR helps support this strategy.

Dopamine on turns: What does the hormone of joy actually do?

How is he involved in decision-making, habit formation, learning, and stress response

The discovery could lead to new treatments.

The researchers note that the work is still at an early stage. The results were obtained in experiments on mice, so it is not yet possible to say that blocking AHR will have the same effect in humans. Before the possible use of the method in medicine, it is necessary to determine how effective protein suppression is in different types of damage to the nervous system, when exactly it should be blocked and what dosages will be safe.

At the same time, the discovery is already of interest for the development of future treatment methods. Some drugs capable of suppressing AHR are already undergoing clinical trials for other diseases. In the future, scientists want to test whether such drugs can be used for peripheral nerve and spinal cord injuries.

The team also plans to explore drug and gene therapy approaches that would reduce AHR activity directly in neurons. The researchers hope to find out if this can enhance axon repair not only after spinal cord injuries, but also in other neurological conditions, including stroke.

So far, the mechanism found cannot be considered as a ready-made treatment. However, he gives scientists a new explanation for why damaged nerves are difficult to repair, and points to a potential point of impact.: instead of forcing the neurons to simply experience the effects of trauma, you can try to switch them to actively repair damaged connections.