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Rett syndrome is one of the neurodevelopmental disorders unique to women.
90%-95% of patients have typical Rett syndrome.
Rett syndrome is caused by mutations or deletions in the MECP2 gene, which encodes methylated CPG binding protein 2.
The typical Rett syndrome can be divided into four stages: in the first stage, approximately between 6 months and 18 months after birth.
About half of children with Rett syndrome have microcephaly or slowed brain growth.
In the second stage, it occurs between the ages of 1 and 4 years old, and functional deterioration occurs.
The skills learned before gradually disappear, and symptoms such as ataxia and sleep disturbance may also occur.
The third stage started between the ages of 2 and 10, and the deterioration of the condition entered a plateau, and seizures appeared.
The fourth stage appears after the age of 10.
This stage lasts for more than ten years or even decades, and symptoms similar to Parkinson's disease, joint contractures, and scoliosis appear.
The treatment of Rett syndrome is currently divided into three main categories: specific symptom treatment (deep brain stimulation therapy to improve learning and memory function), drug therapy (regulation of MeCP2 downstream signals), and gene intervention (still in the experimental stage).
On March 24, 2021, HudaY.
Zoghbi, director of the Jan and Dan Duncan Institute of Neuroscience at Texas Children's Hospital, and professor of the Department of Molecular and Human Genetics, Neurology and Neuroscience at Baylor College of Medicine in the United States, used Rett model mice to reveal Effective exercise training before the occurrence of dyskinesia can effectively alleviate the dysfunction.
Professor HudaY.
Zoghbi has made great contributions to the pathogenesis of neurological diseases including the genetic origin of Rett syndrome, and became known as the "Little Nobel Prize" in 2017.
Recipient of the Galdner Prize. Once considered one of the popular candidates for the Nobel Prize.
Exercise training program Female Rett mice developed dyskinesia at about 12 weeks of age, and this disorder became more and more serious.
Researchers performed exercise training on Rett mice, one group was at 8 weeks of age (before dyskinesias appeared, called early training), and the other group was at 22 weeks of age (after dyskinesias appeared, called post-training) .
Late training can slightly improve the dyskinesia of Rett mice, while early training can significantly improve the dyskinesia.
However, this kind of exercise training can only improve the dyskinesia of Rett mice, and has no effect on other dysfunctions.
Cognitive impairment also exists in Rett syndrome.
Researchers performed water maze training in Rett mice at 4 weeks of age (early training) and (11 weeks of age).
Early training can significantly improve the cognitive dysfunction of Rett mice.
Whether in water maze training or sports training, a group of neurons will be activated, and these activated neurons will be activated again when they receive similar stimuli.
According to the above-mentioned early exercise training can significantly improve the cognitive impairment of Rett mice, the researchers believe that the neurons activated during the training period may be the key to the above-mentioned therapeutic effects.
Chemical genetics inhibits cortex and hippocampal activation of neuron groups.
Researchers used cFOS-cre mice and inhibitory chemical genetics viruses to inhibit their activated neuron groups after early exercise training.
They found that they inhibited the activated neurons.
The colony did not improve the cognitive impairment of Rett mice.
On the other hand, early exercise can promote the complexity of neuronal dendrites in Rett mice, enhance inhibitory postsynaptic currents and excitatory postsynaptic currents, and promote synaptic transmission.
In general, this article found that early exercise intervention can effectively improve motor dysfunction and cognitive impairment in Rett mice.
It is very interesting that this kind of treatment is task-specific, that is, exercise training can only improve motor symptoms, and learning and memory training can only improve cognitive function.
PS: Looking at the complete article, I can only say that the big guy is the big guy! [References] 1.
https://doi.
org/10.
1038/s41586-021-03369-7 The pictures in the article are all from the references
Rett syndrome is one of the neurodevelopmental disorders unique to women.
90%-95% of patients have typical Rett syndrome.
Rett syndrome is caused by mutations or deletions in the MECP2 gene, which encodes methylated CPG binding protein 2.
The typical Rett syndrome can be divided into four stages: in the first stage, approximately between 6 months and 18 months after birth.
About half of children with Rett syndrome have microcephaly or slowed brain growth.
In the second stage, it occurs between the ages of 1 and 4 years old, and functional deterioration occurs.
The skills learned before gradually disappear, and symptoms such as ataxia and sleep disturbance may also occur.
The third stage started between the ages of 2 and 10, and the deterioration of the condition entered a plateau, and seizures appeared.
The fourth stage appears after the age of 10.
This stage lasts for more than ten years or even decades, and symptoms similar to Parkinson's disease, joint contractures, and scoliosis appear.
The treatment of Rett syndrome is currently divided into three main categories: specific symptom treatment (deep brain stimulation therapy to improve learning and memory function), drug therapy (regulation of MeCP2 downstream signals), and gene intervention (still in the experimental stage).
On March 24, 2021, HudaY.
Zoghbi, director of the Jan and Dan Duncan Institute of Neuroscience at Texas Children's Hospital, and professor of the Department of Molecular and Human Genetics, Neurology and Neuroscience at Baylor College of Medicine in the United States, used Rett model mice to reveal Effective exercise training before the occurrence of dyskinesia can effectively alleviate the dysfunction.
Professor HudaY.
Zoghbi has made great contributions to the pathogenesis of neurological diseases including the genetic origin of Rett syndrome, and became known as the "Little Nobel Prize" in 2017.
Recipient of the Galdner Prize. Once considered one of the popular candidates for the Nobel Prize.
Exercise training program Female Rett mice developed dyskinesia at about 12 weeks of age, and this disorder became more and more serious.
Researchers performed exercise training on Rett mice, one group was at 8 weeks of age (before dyskinesias appeared, called early training), and the other group was at 22 weeks of age (after dyskinesias appeared, called post-training) .
Late training can slightly improve the dyskinesia of Rett mice, while early training can significantly improve the dyskinesia.
However, this kind of exercise training can only improve the dyskinesia of Rett mice, and has no effect on other dysfunctions.
Cognitive impairment also exists in Rett syndrome.
Researchers performed water maze training in Rett mice at 4 weeks of age (early training) and (11 weeks of age).
Early training can significantly improve the cognitive dysfunction of Rett mice.
Whether in water maze training or sports training, a group of neurons will be activated, and these activated neurons will be activated again when they receive similar stimuli.
According to the above-mentioned early exercise training can significantly improve the cognitive impairment of Rett mice, the researchers believe that the neurons activated during the training period may be the key to the above-mentioned therapeutic effects.
Chemical genetics inhibits cortex and hippocampal activation of neuron groups.
Researchers used cFOS-cre mice and inhibitory chemical genetics viruses to inhibit their activated neuron groups after early exercise training.
They found that they inhibited the activated neurons.
The colony did not improve the cognitive impairment of Rett mice.
On the other hand, early exercise can promote the complexity of neuronal dendrites in Rett mice, enhance inhibitory postsynaptic currents and excitatory postsynaptic currents, and promote synaptic transmission.
In general, this article found that early exercise intervention can effectively improve motor dysfunction and cognitive impairment in Rett mice.
It is very interesting that this kind of treatment is task-specific, that is, exercise training can only improve motor symptoms, and learning and memory training can only improve cognitive function.
PS: Looking at the complete article, I can only say that the big guy is the big guy! [References] 1.
https://doi.
org/10.
1038/s41586-021-03369-7 The pictures in the article are all from the references
