动物实验 z-bo 2020-11-27 439

　　Damage to fully developed nerve cells can have irreversible consequences, because once nerve fibers mature, they lose their ability to regenerate. New experiments show that activating part of the nerve cell regeneration mechanism, a protein called protrudin (translated as protruding element?), can stimulate the nerves in the eye to re-grow after injury.

　　Glaucoma is a disease in which the optic nerve (connecting the eye and the brain) is damaged and the vision is reduced.

　　"We have achieved the strongest nerve regeneration of all the current technologies." said Keith Martin, an ophthalmologist at the University of Melbourne, Australia. "In the past, it was almost impossible to regenerate the optic nerve, but this study shows the effectiveness of gene therapy in this regard. potential."

　　In 2016, scientists turned on the dormant growth switch to allow adult mice to re-grow a small portion of retinal ganglion cells, and showed that these new nerve cells located at the back of the eye were also reconnected to the right side of the brain.

　　Prior to this, a 2012 study partially restored the "simple" vision in adult blind mice.

　　This latest research is still in its early stages, mainly to understand exactly how protrudin, a scaffold molecule that exists in budding neurons, supports cell growth.

　　Scientists stimulate nerve cells to produce more protrudin to see if it helps to protect cells from damage and even repair them after injury.

　　Researchers have shown that increasing the level of protrudin can stimulate the regeneration of nerve cells cut by laser. Their sparse axons can grow longer and take less time than untreated cells.

　　Next, gene therapy is given to adult mice-injected directly into the eyes-with instructions for the production of nerve cells protrudin. Although it sounds painful, this process can actually be done safely on humans (specifically, the procedure of injection, not to say that gene therapy itself is also safe).

　　Then it was the nerves that deliberately damaged the mice. A few weeks later, more nerve cells survived in the retina of the experimental group of mice than in the control group.

　　In the last experiment, the scientists removed the entire retina of the above experimental group of mice to see if this therapy could prevent the death of nerve cells in the first place.

　　The researchers found that after three days, the stimulation of protrudin produced almost "complete neuroprotection, and these retinas did not show the loss of [retinal] neurons." Generally, about half of the retinal neurons removed in this way will be in Died within a few days.

　　"Our strategy relies on the use of gene therapy-a method that is already in clinical use-to deliver protrudin to the eye." said Veselina Petrova, a neuroscience student at the University of Cambridge. "Our treatment may be further developed. As a means to protect retinal neurons from death and to stimulate their axons to re-grow."

　　It should be noted that animal experiments in a laboratory environment are still a long way from human clinical application.

　　One of the next steps will be to study human retinal cells to see if protrudin has the same protective effect.

　　The scientist who published this work also plans to study whether the same technique can be used to repair neurons damaged after spinal cord injury.

　　"Therapies determined in this way usually show promise in injured spinal cords," Petrova said. "Protrudin that may increase or activate may be used to promote the regeneration of injured spinal cord."