Hope for millions, when paralyzed mice go again after just two weeks of revolutionary gene therapy that regenerates damaged spinal cord nerves
- Paralyzed mice managed to walk two to three weeks after new gene therapy
- Experts have stimulated mouse nerve cells to regenerate using a designer protein
- Nerve cells of the motor-sensory cortex were induced to produce protein
- The mice were then injected with genetic information to create the protein
- The team is now working on new ways to bring treatment to people
An innovative study gave paralyzed mice the ability to walk again, giving hope to approximately 5.4 million people worldwide who suffer from paralysis.
Researchers at the Ruhr Bochum University in Germany stimulated damaged spinal cord nerves in mice to regenerate using a designer protein.
The paralyzed rodents lost their mobility in both hind legs, but after receiving treatment they started walking in just two or three weeks.
The team induced nerve cells in the motor-sensory cortex to produce hyper-interleukin-6.
To do this, they injected genetically modified viruses to “provide the plan for protein production to specific nerve cells.”
Researchers are now exploring whether hyper-interleukin-6 still has positive effects in mice, even though the lesion occurred a few weeks ago, which will allow them to determine if treatment is ready for human studies.
The researchers stimulated the damaged spinal cord nerves of paralyzed mice to regenerate using a designer protein. The paralyzed rodents lost their mobility in both hind legs, but after receiving treatment they started walking in just two or three weeks.
Protein or hyper-interleukin-6 (hIL-6) works by taking on a key feature of spinal cord injuries that cause disability, which is the 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 do communications.
And if these fibers do not recover from an injury, patients suffer from paralysis or numbness of life.
Protein is a cytokine, which is important in cellular 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 in the motor-sensory cortex to produce hyper-interleukin-6. To do this, they injected genetically modified viruses to “provide the plan for protein production to specific nerve cells. Images show a mouse one week after treatment (left) and then eight weeks after (right)
“The special thing about our study is that the protein is not only used to stimulate those nerve cells that produce it on its own, but that it is transported even further (through the brain),” team leader Dietmar Fischer told Reuters.
Research has previously used 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 designer protein.
Fischer and his team used viruses in therapy that stimulated nerve cells in the motor-sensory cortex to produce hIL-6 on its own.
The images show where the injection was targeted during treatment. The team is now working on safe methods for human studies
The viruses were also customized for gene therapy and included plans to make the protein that guides nerve cells, known as motoneurons.
Because these cells are also linked by axonal lateral branches of other nerve cells in other areas of the brain that are important for movement processes, such as walking, hyper-interleukin-6 has also been transported. directly to these essential nerve cells otherwise difficult to access and released there in a controlled manner.
“Thus, the treatment with gene therapy of only a few nerve cells stimulated the axonal regeneration of different nerve cells in the brain and several motor pathways in the spinal cord simultaneously,” says Dietmar Fischer.
“Eventually, this allowed the previously paralyzed animals who received this treatment to start walking after two or three weeks.
“This was a big surprise for us at first, because it was never proven possible before a complete paraplegia.”
The team is now investigating ways to improve the administration of hyper-Interleukin-6, with a view to achieving further functional improvements.
They are also exploring whether hyper-interleukin-6 still has positive effects in mice, even though the lesion occurred a few weeks earlier.
“This aspect would be particularly relevant for application to humans,” Fischer said.
“It simply came to our notice then. These additional experiments will show, among other things, whether it will be possible to transfer these new approaches to humans in the future.