Slightly bumping your head, but there are long-term sequelae such as sleep interruption and epilepsy?

▎The editors of WuXi AppTec's content team have difficulty falling asleep at night, are more and more sensitive to noise and light, daily activities and work are becoming more and more difficult.
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These painful problems may occur after mild head trauma, and It may not appear until months or even years after the initial impact
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With luck, these sequelae may only last for a few days, but there are some cases that can make people suffer for life
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Worldwide, nearly 69 million people are affected by traumatic brain injury each year
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Even mild traumatic brain injury can lead to cognitive and sensory dysfunction, sleep disorders, and epilepsy
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These results are mostly caused by indirect secondary injuries
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The time, location, and manner of secondary injury are essential for the prevention and treatment of traumatic brain injury-related disabilities
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▲Falls, sports injuries, traffic accidents, domestic violence, explosions, etc.
can all cause traumatic brain injury (picture source: 123RF).
In the top academic journal "Science", scientists from the Gladstone Institute in San Francisco, USA published a new article In the paper, the causes of secondary effects of traumatic brain injury are studied
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They pointed out that the complement factor C1q produced by immune cells plays a key role in this process
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The researchers then tried to treat this complement pathway in mouse experiments and found that it can improve the prognosis of traumatic brain injury
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The corresponding author of the paper, Dr.
Jeanne Paz, pointed out: “There is currently no treatment to prevent the disability that may occur after a traumatic brain injury.
How traumatic brain injury affects the brain for a long time is still a gap.
Filling this gap is very important for the development of new and better therapies
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” This This study fills the above gap
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In order to find out the changes related to the secondary effects of brain injury, the researchers first used electrophysiological and wireless cortical recordings to monitor the neurophysiological changes in various brain regions during the various stages of their sleep and wakefulness after the mice experienced mild brain injury.

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After months of observation and analysis, the researchers found that although the main injury site was in the cerebral cortex, in the subsequent time, the thalamus, the deep part of the brain, was disturbed more than the cortex
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What caught their attention in particular was that a molecule called C1q had abnormally high levels in the thalamus in the months following the injury
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Further examination of the human brain tissue obtained by the autopsy, the researchers also found that a few days after suffering from traumatic brain injury, there is a high level of C1q in the human thalamus
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▲Slight traumatic brain injury in the cerebral cortex caused secondary damage to the thalamus (red and blue).
The brain waves of mice during sleep changed from a typical spindle wave to a waveform characteristic of epilepsy (picture source: reference [1] ) C1q is a common inflammatory trigger factor at the injury site, and it is the initiator of the complement cascade in the immune pathway
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Past studies have shown that C1q has a known role in brain development and normal brain function, such as protecting the central nervous system from infection
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In this study, scientists found through mouse models that after brain injury, the immune cells of the central nervous system-microglia continue to produce C1q, causing chronic neuroinflammation, neural circuit dysfunction, and dysfunction in the thalamus.
Neurons die
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Image source: 123RF Based on this discovery, the research team explored ways to avoid chronic brain damage by inhibiting C1q
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"C1q has both good and bad sides.
We want to find a way to prevent the harmful effects of this molecule without affecting its beneficial effects
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" Dr.
Paz said
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To this end, Dr.
Paz collaborated with scientists at the biotechnology company Annexon Biosciences to prepare an antibody to block the activity of the C1q molecule
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They used antibodies to block C1q in time during the "incubation period" after brain trauma in mice, which is the stage where the brain changes but the long-term symptoms have not yet appeared
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The treatment has achieved the expected results: chronic neuroinflammation and thalamic neuron death in the mice have been avoided, and it can be seen that the brain waves of the mice tend to be normal when they sleep
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The researchers pointed out that the timing of treatment is critical
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When they used genetic engineering to make mice lack C1q, they found that the degree of brain damage would be severe
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"This shows that C1q should not be blocked at the stage of brain injury, because it may be important to protect the brain and prevent cell death at this stage
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" Research author Dr.
Stephanie Holden said, "But at a later point in time, block Cutting off C1q can reduce harmful inflammatory responses, just like telling the brain, “It’s okay, you have done the protective part, and now you can turn off inflammation
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” According to reports, the anti-C1q inhibitors developed by Annexon have been used in some to treat themselves.
Application in clinical trials of immune diseases and neurological diseases
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We look forward to the follow-up progress of researchers, which will eventually bring treatments to improve long-term effects for patients with traumatic brain injury
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Reference: [1] Stephanie Holden et al.
, (2021) Complement factor C1q mediates sleep spindle loss and epileptic spikes after mild brain injury.
Science.
Doi: https:// abj2685[2] Preventing the long-term effects of traumatic brain injury.
Retrieved Sep.
10, 2021 from https://medicalxpress.
com/news/2021-09-long-term-effects-traumatic-brain-injury.
html[ 3] Molecular insights into how traumatic brain injury affects the brain in the long term.
Retrieved Sep.
10.
2021 from https://