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Traumatic brain injury (TBI) is one of the main causes of disability in children and adults
.
Every year, TBI affects more than 69 million people worldwide, and may lead to adverse consequences such as cognitive dysfunction, sensory processing difficulties, sleep disruption, and epilepsy
.
Most of them are caused by secondary injury months or years after the occurrence of TBI
.
The primary injury of TBI is irreversible in nature.
Therefore, understanding the time, node, and mechanism of secondary injury is essential to prevent or treat disability after TBI
.
Although the cortex is the main damage site of TBI, secondary damage to the thalamus can also occur, which is mainly manifested as structural changes
.
Studies have shown that these changes are related to many chronic neurodegeneration and inflammation associated with long-term TBI
.
However, most experiments using broad-spectrum anti-inflammatory drugs to improve cognitive impairment in TBI have failed.
This may be because inflammation can cause damage and repair of neuronal circuits
.
Immune factor C1q is the initiator of the classical complement cascade, and it often appears at the site of injury
.
So, what is the role of C1q in corticothalamic system TBI injury? On September 10, 2021, "Science" magazine published online a new achievement from the University of California Jeanne T.
Paz team called "Complement factor C1q mediates sleep spindle loss and epileptic spikes after mild brain injury"
.
They found that complement C1q can mediate sleep spindle loss and epilepsy after TBI
.
Document DOI: 10.
1126/science.
abj2685 In order to explore the role of C1q in the corticothalamic system TBI injury, the researchers used a mild TBI (mTBI) animal model
.
This mTBI does not severely affect the subcortical structure, but it can still cause chronic health problems such as impaired cognition and sleep
.
The results showed that: 3 weeks after mTBI injury in mice, chronic inflammation and neuronal loss occurred in the cortex and its function-related thalamus, and the expression of C1q increased
.
Increased C1q expression and neuron loss in mTBI mice To determine the source of C1q cells in the thalamus, the researchers performed microdissections on nRT and VB thalamus tissues after 3 weeks of injury
.
Single-cell sequencing showed that microglia are the source of C1q in the thalamus
.
Subsequently, the researchers used specific antibody binding to block C1q 3 weeks after mTBI, and found that its chronic inflammation and neuron loss were reduced
.
This indicates that C1q is an important regulator of the subsequent disease occurrence of mTBI
.
After anti-C1q treatment, mTBI mice have decreased C1q and decreased neuron loss.
In mTBI animal models, sleep spindle loss and increased epilepsy peaks will also occur
.
The researchers applied anti-C1q treatment to mTBI mice, which significantly restored the reduction in spindle waves and reduced focal epileptic activity
.
Reduced sleep spindle loss in mTBI mice after anti-C1q treatment.
In summary, the increase in C1q expression is related to neuron loss and chronic inflammation, and is related to the destruction of sleep spindles, EEG signs in the early stages of sleep, and the development of epileptic activity
.
Blocking C1q can offset the above-mentioned adverse consequences
.
Because the thalamus is connected to the cortex, the thalamus is likely to be the site of secondary injury
.
Therefore, the corticothalamus circuit may become a new target for the treatment of TBI-related diseases
.
End reference materials: [1]https://
.
Every year, TBI affects more than 69 million people worldwide, and may lead to adverse consequences such as cognitive dysfunction, sensory processing difficulties, sleep disruption, and epilepsy
.
Most of them are caused by secondary injury months or years after the occurrence of TBI
.
The primary injury of TBI is irreversible in nature.
Therefore, understanding the time, node, and mechanism of secondary injury is essential to prevent or treat disability after TBI
.
Although the cortex is the main damage site of TBI, secondary damage to the thalamus can also occur, which is mainly manifested as structural changes
.
Studies have shown that these changes are related to many chronic neurodegeneration and inflammation associated with long-term TBI
.
However, most experiments using broad-spectrum anti-inflammatory drugs to improve cognitive impairment in TBI have failed.
This may be because inflammation can cause damage and repair of neuronal circuits
.
Immune factor C1q is the initiator of the classical complement cascade, and it often appears at the site of injury
.
So, what is the role of C1q in corticothalamic system TBI injury? On September 10, 2021, "Science" magazine published online a new achievement from the University of California Jeanne T.
Paz team called "Complement factor C1q mediates sleep spindle loss and epileptic spikes after mild brain injury"
.
They found that complement C1q can mediate sleep spindle loss and epilepsy after TBI
.
Document DOI: 10.
1126/science.
abj2685 In order to explore the role of C1q in the corticothalamic system TBI injury, the researchers used a mild TBI (mTBI) animal model
.
This mTBI does not severely affect the subcortical structure, but it can still cause chronic health problems such as impaired cognition and sleep
.
The results showed that: 3 weeks after mTBI injury in mice, chronic inflammation and neuronal loss occurred in the cortex and its function-related thalamus, and the expression of C1q increased
.
Increased C1q expression and neuron loss in mTBI mice To determine the source of C1q cells in the thalamus, the researchers performed microdissections on nRT and VB thalamus tissues after 3 weeks of injury
.
Single-cell sequencing showed that microglia are the source of C1q in the thalamus
.
Subsequently, the researchers used specific antibody binding to block C1q 3 weeks after mTBI, and found that its chronic inflammation and neuron loss were reduced
.
This indicates that C1q is an important regulator of the subsequent disease occurrence of mTBI
.
After anti-C1q treatment, mTBI mice have decreased C1q and decreased neuron loss.
In mTBI animal models, sleep spindle loss and increased epilepsy peaks will also occur
.
The researchers applied anti-C1q treatment to mTBI mice, which significantly restored the reduction in spindle waves and reduced focal epileptic activity
.
Reduced sleep spindle loss in mTBI mice after anti-C1q treatment.
In summary, the increase in C1q expression is related to neuron loss and chronic inflammation, and is related to the destruction of sleep spindles, EEG signs in the early stages of sleep, and the development of epileptic activity
.
Blocking C1q can offset the above-mentioned adverse consequences
.
Because the thalamus is connected to the cortex, the thalamus is likely to be the site of secondary injury
.
Therefore, the corticothalamus circuit may become a new target for the treatment of TBI-related diseases
.
End reference materials: [1]https://
