The silver lining for millions of people as paralyzed mice revives damaged spinal nerves due to re-iteration of gene therapy just twice
- Paralyzed rats were able to walk two to three weeks after a new gene therapy
- Experts stimulate mice’s nerve cells to regenerate using a designer protein
- Nerve cells of the motor-sensory cortex were stimulated to produce proteins
- The mice were then given genetic information to make proteins
- The team is now working on new methods to treat humans
A ground-breaking study has given paralyzed mice the ability to walk again, causing approximately 5.4 million people worldwide to suffer from paralysis.
Researchers at Ruhr University Bochum in Germany stimulated the damaged spinal nerves of mice to regenerate using a designer protein.
Paralyzed rodents had lost mobility in both legs, but started walking in just two to three weeks after receiving treatment.
The team induced nerve cells of the motor-sensory cortex to produce hyper-interleukin-6.
To do this, they injected genetically engineered viruses to ‘deliver blueprint to the production of proteins to specific nerve cells’.
Researchers are now exploring whether hyper-interleukin-6 still has a positive effect in mice, even if the injury occurred several weeks earlier, which would allow them to determine if the treatment is ready for human trials.
Researchers prompted damaged spinal nerves of paralyzed mice to regenerate using a designer protein. Paralyzed rodents had lost mobility in both legs, but started walking in just two to three weeks after receiving treatment
Protein, or hyper-interleukin-6 (HIL-6) is a major feature of spinal cord injuries that cause disabilities, which operate by damaging the nerve fibers known as axons. .
Exons send signals back and forth between the brain, skin, and muscles, and when they stop working, it communicates.
And if these fibers do not recover from any injury, then patients suffer paralysis or numbness of life.
The protein is a cytokine, important in cell signaling, but being a ‘designer’ means that it is not found in nature and can only be produced using genetic engineering.
The team induced nerve cells of the motor-sensory cortex to produce hyper-interleukin-6. To do this, they injected genetically engineered viruses to give specific nerve cells a blueprint for protein production. The picture shows a mouse one week after treatment (left) and then eight weeks later (right)
Dietmar Fisher, the head of the team, told Reuters in an interview that the special thing about our study is that the protein is used not only to stimulate the nerve cells that produce it themselves, but also that It is also transported further (through the brain).
Research previously used a similar gene therapy to regenerate nerve cells in the visual system, but more recent studies focused on those in the motor-sensory cortex that produce designer proteins.
Fisher and his team used the virus in therapy, which stimulates nerve cells in the motor-sensory cortex, to form hIL-6 on its own.
The pictures show where the injection was targeted during treatment. The team is now working on ways to safely test humans
The virus was also adapted for gene therapy and included blueprints for creating proteins to guide nerve cells, known as precursors.
Since these cells also bind to other nerve cells in other brain regions via axonal side branches that are important for important processes such as the process of moving, hyper-interleukin-6 was also directly transported to them. , Otherwise it becomes difficult to reach the required nerve cells and left there. In a controlled manner.
Detmar Fisher explains, ‘Thus, gene therapy treatment of only a few nerve cells stimulated axonal regeneration of several nervous systems in the brain and spinal cord’.
Ultimately, this enabled earlier paralyzed animals who started walking after two to three weeks.
‘It was very surprising to us in the beginning, as it has never been shown before after complete paraplegia.’
With the goal of achieving additional functional improvements, the team is now investigating ways to improve the administration of hyper-interleukin-6.
They are also exploring whether hyper-interleukin-6 still has a positive effect in mice, even if the injury occurred several weeks earlier.
‘This aspect will be particularly relevant for application in humans,’ Fisher said.
‘We are now breaking new scientific grounds. These further experiments will show, among other things, whether it will be possible in future to transfer these new approaches to humans. ‘