Traumatic injuries affecting the central nervous system (CNS), including those to the brain, spinal cord, and optic nerve, are the leading cause of disability and the second leading cause of death worldwide. CNS lesions often result in significant loss of sensory, motor, and visual functions, presenting a challenge for physicians and scientists researching to find a solution.
Visual dysfunction linked to optic nerve injury could be reversed thanks to the finding by a team of neuroscientists at the City University of Hong Kong (CityU) that they have identified a small therapeutic molecule –M1– that can stimulate nerve regeneration and restore visual functions in the mammalian central nervous system, a finding that offers great hope for patients with optic nerve injury, such as glaucoma-associated vision loss.
“There is currently no effective treatment available for traumatic CNS injuries, so there is an immediate need for a potential drug to promote CNS repair and ultimately achieve full recovery of function, such as visual function. , in patients,” said Dr. Eddie Ma Chi, Associate Chair and Associate Professor in the Department of Neuroscience and Director of the Laboratory Animal Research Unit at CityU, who led the research.
Potential treatment for glaucoma or diabetic retinopathy
The results of the study have been published in the Proceedings of the National Academy of Sciences (PNAS) and represent a new therapeutic approach to accelerate functional recovery after CNS lesions. The M1 molecule, researchers have shown, stimulates the fusion and motility of mitochondria (a cell’s powerhouse for energy) and induces robust axon regeneration by enhancing the intrinsic growth capacity of injured neurons.
“Successful restoration of visual function was observed only in M1-treated mice four to six weeks after optic nerve damage”
The photoreceptors in the eyes [retina] send visual information to neurons in the retina. To facilitate recovery of visual function after injury, the axons of neurons must regenerate via the optic nerve and transmit nerve impulses to visual targets in the brain via the optic nerve for imaging and processing. , explained Dr. Ma.
“M1 treatment sustains long-distance axon regeneration from the optic chiasm, i.e., halfway between the eyes and the target brain region, to multiple subcortical visual targets in the brain. The regenerated axons elicit neural activities in the targeted brain regions and restore visual functions after M1 treatment. Our study highlights the potential of a readily available, non-viral therapy for CNS repair.”
The study has lasted seven years and is based on the previous investigation of this team of scientists on the regeneration of peripheral nerves through gene therapy. “This time we have used the small molecule M1 to repair the CNS simply by intravitreal injection into the eyes, which is an established medical procedure for patients, that is, for the treatment of macular degeneration. Successful restoration of visual function, such as pupillary light reflex and responses to impending visual stimuli, eg, visually induced innate defensive responses to avoid predators, was observed only in M1-treated mice aged four to six weeks after the optic nerve was damaged,” said Dr. Au Ngan-pan, a research associate in the Department of Neuroscience.
Researchers are developing an animal model to treat glaucoma-related vision loss using M1, which may also prove useful in the treatment of other eye diseases and visual impairments such as diabetic retinopathy, macular degeneration, and traumatic optic neuropathy, for example. which they consider necessary to carry out new studies to evaluate the possible clinical application of M1. “Nerve regeneration and recovery of function will help improve the quality of life for patients and reduce the burden on the local community and healthcare systems,” concludes Dr. Ma.
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