A study published in Science claims to have found the genetic pathways and mechanisms responsible for the suppression of neuronal regeneration in mammalian neurons and how to repress those mechanisms to aid in neuronal regeneration after axonal injuries.
A neuron is the basic working unit of the brain, much like the cells in the rest of the body. These working units are important for the transmission of signals and information from the brain to other neurons, or to muscles and tissues in the body.
Damage to neurons is extremely detrimental to one’s health as they are very important for the normal functioning of the body. Furthermore, damage to neurons is often permanent as neurons are famously known for their inability to regenerate.
However, this is a feature shared by all mammalian species. Neurons in the mammalian nervous system are unable to regenerate after injury but can regenerate effectively during the developmental process. Many studies are being performed to better understand the mechanism behind this inability.
A University of Notre Dame Study
One such study was performed with the objective of understanding the retinal neuronal regeneration process in vertebrates like zebrafish and apply that information to the mammalian retinal neuronal death or regeneration process.
The study was conducted by a team of researchers from the University of Notre Dame, Johns Hopkins University, Ohio State University, and the University of Florida and was led by Hoang and Wang from the Johns Hopkins University School of Medicine Department of neuroscience and department of ophthalmology respectively.
The researchers studied the involvement of specific cells called Muller glia in the regeneration process of vertebral retinal neurons. Muller glia are specific cells found in the brain which are responsible for neuronal regeneration through a specific process called, reprogramming. Humans also have the Muller glia cells but these cells do not function similarly to those in zebrafish. In fact, they respond by initiating the gliosis or scar forming process in humans after neuronal injury.
Hence, the researchers tried to identify the gene regulatory networks responsible for the functioning of Muller glia in the animal models like zebrafish, and chicken and then tried to profile these changes in the same animal models to apply them to the mammalian animal model’s genetic pathways.
Results of the study
Huang and his team found that animal models like zebrafish and chicken showed conserved and species-specific gene networks that control the glial quiescence, reactivity, and neurogenesis important for neuronal and retinal regeneration.
However, in the mammalian animal models like mice, they found that a direct transition from quiescence to reactivity, like that seen in zebrafish, is not possible and these models were incapable of regeneration due to a dedicated gene network that suppresses neurogenic competence and restores quiescence. This gene network is what was studied and manipulated by a team of researchers to make retinal regeneration a possibility.
The researchers found that the disruption of transcription factors responsible for the restoration of quiescence is responsible for the stimulation of Muller glia cell proliferation which then results in retinal regeneration.
This study conclusively proves that retinal regeneration is possible in mammalian brain cells or neurons and the researchers are now trying to apply these findings to design new therapies for nervous system disorders that cause retinal degeneration. They are also trying to replicate these findings in the brain neurons.
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