-
Categories
-
Pharmaceutical Intermediates
-
Active Pharmaceutical Ingredients
-
Food Additives
- Industrial Coatings
- Agrochemicals
- Dyes and Pigments
- Surfactant
- Flavors and Fragrances
- Chemical Reagents
- Catalyst and Auxiliary
- Natural Products
- Inorganic Chemistry
-
Organic Chemistry
-
Biochemical Engineering
- Analytical Chemistry
-
Cosmetic Ingredient
- Water Treatment Chemical
-
Pharmaceutical Intermediates
Promotion
ECHEMI Mall
Wholesale
Weekly Price
Exhibition
News
-
Trade Service
Click on the blue to pay attention to us.
Traumatic brain injury (TBI) is the main cause of disability in children and adults.
It can cause cognitive dysfunction, sensory processing difficulties, sleep difficulties and epilepsy
.
Most of these adverse consequences occur months or years after TBI and are caused by indirect secondary injuries
.
Because the cortex is located below the skull, it is the most directly damaged part of traumatic brain injury, and the thalamus becomes the main part of secondary damage.
This may be because it has a close and long-distance connection with the cerebral cortex
.
Chronic neuroimmune response is more likely to occur in the site of secondary injury, and the complement pathway is one of the signal pathways that regulate this neuroinflammation
.
Complement activation promotes inflammation and neurotoxicity of central nervous system damage
.
On September 10, 2021, the Jeanne T.
Paz research team at the University of California found that the expression of complement C1q was up-regulated in the cortex and thalamus through a model of chronic traumatic brain injury.
This increase is related to neuronal loss, sleep disturbance, and epileptic activity
.
Reducing the expression of C1q can effectively alleviate the above symptoms
.
After traumatic brain injury, C1q accumulates abnormally, and glial cell inflammation occurs.
Researchers built a traumatic brain injury model in the right primary somatosensory cortex (S1) of mice.
After 3 weeks, the expression of complement C1q in the S1 area increased.
The number of cells decreases, showing glial inflammation (the number of microglia and astrocytes increases)
.
The ventral basal thalamus and reticulothalamic nucleus, which are functionally connected to the S1 area, also have the above-mentioned lesions
.
Electrophysiological experiments found that the spontaneous excitability and inhibitory postsynaptic currents of the reticularthalamic nucleus were reduced after traumatic brain injury, indicating that there is a synaptic transmission dysfunction in this brain area, but this synaptic function is not found in the ventral basal thalamus Obstacles
.
Previous studies have shown that complement C1q/C3 can promote the loss of synapses and cause synaptic dysfunction
.
Further, through single-cell sequencing, it was found that C1q in the brain region of the reticularthalamic nucleus was mainly derived from microglia, while astrocytes and oligodendrocytes were the source of complement C4b
.
Reducing C1q levels by neutralizing antibodies can reduce glial cell inflammation and reduce neuronal loss in mice with traumatic brain injury
.
This result has also been further verified in C1q knockout mice
.
Lowering the level of C1q can improve brain damage caused by sleep disorders.
Sleep spindle is a brain rhythm activity produced in the reticulothalamic nucleus during non-rapid eye movement sleep
.
After traumatic brain injury, the sleep spindle of the cortex is reduced, and epileptic activity appears
.
After reducing the level of C1q by neutralizing antibodies, this obstacle can be significantly improved
.
This paper found that chronic traumatic brain injury specifically caused synaptic dysfunction in the reticularthalamic nucleus and abnormal accumulation of complement C1q
.
After reducing the expression of C1q, it can effectively alleviate sleep disorders and epileptiform activities caused by trauma
.
Complement C1q has become a potential target for the treatment of brain trauma
.
At present, the United States Annexon Biosciences company has developed a strong C1q monoclonal antibody ANX005, which is approved by the US FDA to treat Guillain-Barré syndrome
.
Inhibitors related to the complement pathway pathway are mainly used to treat rare diseases.
The research found in this article has further expanded the drug application of complement C1q inhibitors, and is expected to become a clinical drug for the treatment of traumatic brain injury in the future
.
[References] 1.
https://doi.
org/10.
1126/science.
abj2685 The pictures in the text are from the references
Traumatic brain injury (TBI) is the main cause of disability in children and adults.
It can cause cognitive dysfunction, sensory processing difficulties, sleep difficulties and epilepsy
.
Most of these adverse consequences occur months or years after TBI and are caused by indirect secondary injuries
.
Because the cortex is located below the skull, it is the most directly damaged part of traumatic brain injury, and the thalamus becomes the main part of secondary damage.
This may be because it has a close and long-distance connection with the cerebral cortex
.
Chronic neuroimmune response is more likely to occur in the site of secondary injury, and the complement pathway is one of the signal pathways that regulate this neuroinflammation
.
Complement activation promotes inflammation and neurotoxicity of central nervous system damage
.
On September 10, 2021, the Jeanne T.
Paz research team at the University of California found that the expression of complement C1q was up-regulated in the cortex and thalamus through a model of chronic traumatic brain injury.
This increase is related to neuronal loss, sleep disturbance, and epileptic activity
.
Reducing the expression of C1q can effectively alleviate the above symptoms
.
After traumatic brain injury, C1q accumulates abnormally, and glial cell inflammation occurs.
Researchers built a traumatic brain injury model in the right primary somatosensory cortex (S1) of mice.
After 3 weeks, the expression of complement C1q in the S1 area increased.
The number of cells decreases, showing glial inflammation (the number of microglia and astrocytes increases)
.
The ventral basal thalamus and reticulothalamic nucleus, which are functionally connected to the S1 area, also have the above-mentioned lesions
.
Electrophysiological experiments found that the spontaneous excitability and inhibitory postsynaptic currents of the reticularthalamic nucleus were reduced after traumatic brain injury, indicating that there is a synaptic transmission dysfunction in this brain area, but this synaptic function is not found in the ventral basal thalamus Obstacles
.
Previous studies have shown that complement C1q/C3 can promote the loss of synapses and cause synaptic dysfunction
.
Further, through single-cell sequencing, it was found that C1q in the brain region of the reticularthalamic nucleus was mainly derived from microglia, while astrocytes and oligodendrocytes were the source of complement C4b
.
Reducing C1q levels by neutralizing antibodies can reduce glial cell inflammation and reduce neuronal loss in mice with traumatic brain injury
.
This result has also been further verified in C1q knockout mice
.
Lowering the level of C1q can improve brain damage caused by sleep disorders.
Sleep spindle is a brain rhythm activity produced in the reticulothalamic nucleus during non-rapid eye movement sleep
.
After traumatic brain injury, the sleep spindle of the cortex is reduced, and epileptic activity appears
.
After reducing the level of C1q by neutralizing antibodies, this obstacle can be significantly improved
.
This paper found that chronic traumatic brain injury specifically caused synaptic dysfunction in the reticularthalamic nucleus and abnormal accumulation of complement C1q
.
After reducing the expression of C1q, it can effectively alleviate sleep disorders and epileptiform activities caused by trauma
.
Complement C1q has become a potential target for the treatment of brain trauma
.
At present, the United States Annexon Biosciences company has developed a strong C1q monoclonal antibody ANX005, which is approved by the US FDA to treat Guillain-Barré syndrome
.
Inhibitors related to the complement pathway pathway are mainly used to treat rare diseases.
The research found in this article has further expanded the drug application of complement C1q inhibitors, and is expected to become a clinical drug for the treatment of traumatic brain injury in the future
.
[References] 1.
https://doi.
org/10.
1126/science.
abj2685 The pictures in the text are from the references
