We expect millions of paralyzed mice to walk again after TWO WEEKS of innovative gene therapy that regenerates damaged spinal cord nerves
- The paralyzed mice were able to walk two or three weeks after a new gene therapy
- Experts stimulated the regeneration of nerve cells in mice using a design protein
- Nerve cells in the motor-sensory cortex were induced to produce the protein
- Genetic information was then injected into the mice to create the protein
- The team is now working on new methods to get the treatment to humans
An innovative study has given paralyzed mice the ability to walk again, providing hope to some 5.4 million people suffering from paralysis worldwide.
Researchers at Ruhr University in Bochum, Germany, stimulated the regeneration of damaged spinal cord nerves in mice using a design protein.
The paralyzed rodents had lost mobility in both hind legs, but after receiving treatment they began to walk in just two or three weeks.
The team induced nerve cells in the motor-sensory cortex to produce hyper-interleukin-6.
To do so, they injected genetically modified viruses to “deliver the plan for protein production to specific nerve cells.”
Researchers are now exploring whether hyper-interleukin-6 still has positive effects in mice, even if the lesion occurred several weeks earlier, which will allow them to determine if treatment is ready for trials in humans.
The researchers stimulated damaged spinal cord nerves from paralyzed mice to regenerate using a design protein. The paralyzed rodents had lost mobility in both hind legs, but after receiving treatment they began to walk in just two or three weeks.
The protein, or hyper-interleukin-6 (hIL-6), acts by taking a key feature of spinal cord injuries that produce disability, which is damage to nerve fibers known as axons.
Axons send signals 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 cell signaling, but being a “designer” means it is not found in nature and can only be produced by genetic engineering.
The team induced nerve cells in the motor-sensory cortex to produce hyper-interleukin-6. To do so, they injected genetically modified viruses to “deliver the plan for protein production to specific nerve cells. The images show a mouse one week after treatment (left) and then eight weeks later (right).
“The special thing about our study is that the protein is not only used to stimulate the nerve cells that produce it themselves, but it is also carried further (through the brain),” he told Reuters, the team leader Dietmar Fischer.
Previously, research 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 the design protein.
Fischer and his team used viruses in therapy that stimulated motor-sensory cortex nerve cells to make hIL-6 on their own.
The images show where the injection was directed during treatment. The team is now working on methods to conduct tests safely on humans
The viruses were also customized for gene therapy and included blueprints to make the protein that guides nerve cells, known as motoneurons.
Since these cells also bind through axonal lateral branches to other nerve cells in other brain areas that are important for movement processes such as walking, hyper-interleukin-6 was also transported directly to these essential nerve cells otherwise difficult to access in a controlled manner.
“Thus, treatment with gene therapy of a few nerve cells stimulated the axonal regeneration of several nerve cells in the brain and several motor pathways in the spinal cord simultaneously,” notes Dietmar Fischer.
“Ultimately, this allowed the previously paralyzed animals receiving this treatment to start walking after two or three weeks.
“That was a big surprise for us at first, as it had never been shown to be possible after a complete paraplegia.”
The team is now investigating ways to improve the administration of hyper-interleukin-6, with the goal of achieving additional functional improvements.
They are also exploring whether hyper-interleukin-6 still has positive effects in mice, even if the lesion occurred several weeks earlier.
“This aspect would be particularly relevant for application in humans,” Fischer said.
“We are now opening up new scientific bases. These subsequent experiments will show, among other things, whether it will be possible to transfer these new approaches to humans in the future. “