Science is uncharacteristic!

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iNature Traumatic Brain Injury (TBI) is the main cause of disability in children and adults
.

TBI affects 69 million people worldwide each year and can cause cognitive dysfunction, sensory processing difficulties, sleep disruption, and epilepsy
.

Most of these adverse consequences occur months or years after TBI and are caused by indirect secondary injuries, which are the consequences of the initial impact
.

Since the primary injury is irreversible in nature, understanding where, when, and how the secondary injury occurs is essential to prevent or treat disability after TBI
.

On September 10, 2021, the JEANNE T.
PAZ team from the University of California, San Francisco published a research paper titled "Complement factor C1q mediates sleep spindle loss and epileptic spikes after mild brain injury" in Science.
The study used mild TBI (mTBI).
) In the mouse model of the cortico-thalamic system with chronic increases in C1q expression
.

Increased expression of C1q coexists with neuronal loss and chronic inflammation, and is associated with the interruption of sleep spindles and the appearance of epileptic activity
.

Blocking C1q offset these results, indicating that C1q is a disease modulator in mTBI
.

Mononuclear RNA sequencing indicated that microglia are the source of thalamic C1q
.

Therefore, the corticothalamus circuit may become a new target for the treatment of TBI-related disabilities
.

Traumatic brain injury (TBI) is the main cause of disability in children and adults
.

TBI affects 69 million people worldwide each year and can cause cognitive dysfunction, sensory processing difficulties, sleep disruption, and epilepsy
.

Most of these adverse results occur months or years after TBI and are caused by indirect secondary injuries that are the consequence of the initial impact
.

Since the primary injury is irreversible in nature, understanding where, when, and how the secondary injury occurs is essential to prevent or treat disability after TBI
.

The cortex is usually the site of the primary injury because it is located directly below the skull
.

However, the cortex belongs to many larger circuits, especially the cortex-thalamic-cortical ring
.

This circuit is important for sensory processing, attention, cognition and sleep
.

Although the thalamus itself is not acutely injured in TBI, it will experience secondary damage, which may be due to its long-distance interconnection with the cerebral cortex
.

The structural changes of the thalamus are associated with many long-term health outcomes related to TBI, and TBI patients exhibit secondary and chronic neurodegeneration and inflammation in the thalamic nucleus
.

Chronic neuroinflammation is common at the site of secondary injury, but most attempts to improve cognitive outcomes after TBI with a wide range of anti-inflammatory drugs have failed
.

One potential mediator of inflammation and injury after TBI is the complement pathway, which is activated in the area surrounding the injury of brain injury
.

Complement activation leads to inflammation and neurotoxicity of central nervous system (CNS) damage, and is increased in human brains with injury, epilepsy, and Alzheimer's disease
.

Abnormal activation of C1 (the starting molecule of the classical complement cascade) can trigger the elimination of synapses and promote the progression of neurodegenerative diseases
.

In contrast, C1/C1q is involved in normal synaptic pruning during development, and the complement system plays an important role in brain homeostasis by removing cell debris and protecting the CNS from infection
.

This study explored the role of C1q in the TBI injury of corticothalamic system function, with special emphasis on the time and location of C1q expression
.

The study used a mild TBI (mTBI) mouse model that does not severely affect the subcortical structure, and used cell electrophysiology and wireless cortical recording to monitor neurophysiological changes in various areas of the cortex and thalamus in free-behaving mice
.

The study used a mouse model of mild TBI (mTBI) and found a chronic increase in C1q expression in the corticothalamus
.

 Increased expression of C1q coexists with neuronal loss and chronic inflammation, and is associated with the interruption of sleep spindles and the appearance of epileptic activity
.

 Blocking C1q offset these results, indicating that C1q is a disease modulator in mTBI
.

 Mononuclear RNA sequencing indicated that microglia are the source of thalamic C1q
.

 Therefore, the corticothalamus circuit may become a new target for the treatment of TBI-related disabilities
.

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