Hope for millions when paralyzed mice walk again after just TWO WEEKS of breakthrough gene therapy that regenerates damaged spinal nerves
- Paralyzed mice were able to walk for two to three weeks after a new gene therapy
- Experts stimulated the mice’s nerve cells to regenerate with the help of a designer protein
- Nerve cells of the motor sensory cortex were induced to produce the protein
- The mice were then injected with genetic information to make the protein
- The team is now working on new methods of delivering the treatment to humans
A groundbreaking study has given paralyzed mice the opportunity to walk again, offering hope to approximately 5.4 million people worldwide who suffer from paralysis.
Researchers at Ruhr University Bochum in Germany stimulated the damaged nerves of the mice’s spinal cords to regenerate with the help of a designer protein.
The paralyzed rodents had lost mobility in both hind legs, but started walking within two to three weeks after 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 the blueprint for the production of the protein to specific nerve cells.”
Researchers are now investigating whether hyperinterleukin-6 still has positive effects in mice, even if the injury occurred several weeks earlier, allowing them to determine if the treatment is ready for human trials.
Researchers stimulated the damaged nerves of the paralyzed mice’s spinal cords to regenerate with the help of a designer protein. The paralyzed rodents had lost mobility in both hind legs, but after treatment they started walking within two to three weeks
The protein, or hyper-interleukin-6 (hIL-6), works by assuming an important characteristic of spinal cord injuries that cause disability, namely damage to nerve fibers known as axons.
Axons send signals back and forth between the brain, skin, and muscles, and when they stop working, so does communication.
And if these fibers don’t recover from injury, patients suffer from paralysis or numbness.
The protein is a cytokine, which is important in cell signaling, but because it is a ‘designer’ it does not occur in nature and can only be produced by 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 “deliver the blueprint for the production of the protein to specific nerve cells.” Pictures show a mouse one week after treatment (left) and then eight weeks after (right)
‘The special thing about our research is that the protein is not only used to stimulate those nerve cells that make it themselves, but that it is also transported further (through the brain),’ team leader Dietmar Fischer told Reuters in an interview.
Studies previously used a similar gene therapy to regenerate nerve cells in the visual system, but the recent study focused on those in the motor-sensory cortex to produce the designer protein.
Fischer and his team used viruses in the therapy that stimulated nerve cells in the motor-sensory cortex to make hIL-6 themselves.
The images show where the injection was aimed during the treatment. The team is now working on methods to conduct safe human trials
The viruses were also adapted for gene therapy and contained blueprints for making the protein to direct the nerve cells, known as motor neurons.
Because these cells are also connected via axonal side branches to other nerve cells in other areas of the brain that are important for movement processes such as walking, the hyperinterleukin-6 was also transported directly to these otherwise difficult to reach essential nerve cells and released there. in a controlled manner.
“Gene therapy treatment of only a few nerve cells thus stimulated the axonal regeneration of different nerve cells in the brain and multiple motor channels in the spinal cord at the same time,” says Dietmar Fischer.
This allowed the previously paralyzed animals that received this treatment to eventually start walking after two to three weeks.
“This came as a big surprise to us at first, as it had never been possible after a complete spinal cord injury.”
The team is now exploring ways to improve the administration of hyper-interleukin-6, with the aim of achieving additional functional improvements.
They are also investigating whether hyper-interleukin-6 still has positive effects in mice, even if the injury occurred several weeks earlier.
“This aspect would be especially relevant for human application,” said Fischer.
‘We are now pioneering in science. These further experiments will reveal, among other things, whether it will be possible to transfer these new approaches to humans in the future. ‘