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News from March 11, 2021 //---Traumatic brain injury (TBI) is the main cause of disability and a risk factor for early-onset dementia.
It is characterized by damage to the body, followed by neuroinflammation driven by complement.
Complement is a part of the innate immune system, which plays a role in the brain and the entire body.
It can enhance the body's ability to resist pathogens, promote inflammation and remove damaged cells.
Complement plays an important role in the brain.
Whether it is infected or injured, it affects the development of the brain and the formation of synapses.
It is characterized by damage to the body, followed by neuroinflammation driven by complement.
Complement is a part of the innate immune system, which plays a role in the brain and the entire body.
It can enhance the body's ability to resist pathogens, promote inflammation and remove damaged cells.
Complement plays an important role in the brain.
Whether it is infected or injured, it affects the development of the brain and the formation of synapses.
In TBI, complement-induced inflammation determines the outcome of the patient to a certain extent within a few weeks after injury.
However, more research is needed to determine the role of the complement system in neurodegeneration after craniocerebral injury, especially in the long-term chronic phase of TBI.
In addition, treatment of TBI patients is limited to the acute phase after injury, because the link between the initial insult and chronic neurodegeneration and subsequent months and years of cognitive decline is poorly understood.
However, more research is needed to determine the role of the complement system in neurodegeneration after craniocerebral injury, especially in the long-term chronic phase of TBI.
In addition, treatment of TBI patients is limited to the acute phase after injury, because the link between the initial insult and chronic neurodegeneration and subsequent months and years of cognitive decline is poorly understood.
Researchers at the Medical University of South Carolina (MUSC), Ralph H.
Johnson VA Medical Center and elsewhere have reported a link between the complement system and the chronic phase of TBI.
Their results were published online on January 12 in the Journal of Neuroscience, and the results showed that inhibition of complement two months after TBI disrupted neurodegeneration and improved cognitive function.
Johnson VA Medical Center and elsewhere have reported a link between the complement system and the chronic phase of TBI.
Their results were published online on January 12 in the Journal of Neuroscience, and the results showed that inhibition of complement two months after TBI disrupted neurodegeneration and improved cognitive function.
"The vast majority of studies that study different therapies in TBI are done with acute therapy within a few hours after the acute attack.
Our research is of great significance because we will start treatment two months after TBI.
"
Our research is of great significance because we will start treatment two months after TBI.
"
(Image source:style="text-align: justify;">In order to understand the timing of complement and chronic TBI more comprehensively, the author first studied the body's response to the damaged part.
They found that certain brain cells called microglia disrupted synapses characterized by complement.
This process reduces the total number and density of synapses in the brain.
In addition, they reported sustained complement activation for up to three months after a TBI injury, and expanded neuroinflammation throughout the brain area.
This inflammatory response promotes the degeneration of synapses and heralds progressive cognitive decline.
They found that certain brain cells called microglia disrupted synapses characterized by complement.
This process reduces the total number and density of synapses in the brain.
In addition, they reported sustained complement activation for up to three months after a TBI injury, and expanded neuroinflammation throughout the brain area.
This inflammatory response promotes the degeneration of synapses and heralds progressive cognitive decline.
The researchers then studied the therapeutic effects of blocking complement.
They used a complement inhibitor that specifically targets areas of complement activation and brain cell damage.
Inhibition of complement interrupted the decline in brain cell function and reversed mental loss in the task of assessing spatial learning and memory, even if the administration of the inhibitor was postponed to two months after the injury.
They used a complement inhibitor that specifically targets areas of complement activation and brain cell damage.
Inhibition of complement interrupted the decline in brain cell function and reversed mental loss in the task of assessing spatial learning and memory, even if the administration of the inhibitor was postponed to two months after the injury.
The author of the article, Tomlinson, said: "A major advantage of our approach is that we do not systematically inhibit complement activity.
Acute therapy is not a big problem, but long-term treatment of patients with complement inhibitors systematically is not the best choice, because Complement also has other important functions, from host defense to controlling homeostasis and regeneration mechanisms.
"
Acute therapy is not a big problem, but long-term treatment of patients with complement inhibitors systematically is not the best choice, because Complement also has other important functions, from host defense to controlling homeostasis and regeneration mechanisms.
"
So far, treatment research in preclinical models has almost completely focused on the acute treatment of TBI.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
These findings are critical because rehabilitation intervention is the only management strategy available for TBI to improve cognitive and motor function.
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
Source of information: com/news/2021-03-complement-inhibition-reverses-mental-losses.
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
Original source: Ali Alawieh et al, Complement Drives Synaptic Degeneration and Progressive Cognitive Decline in the Chronic Phase after Traumatic Brain Injury, The Journal of Neuroscience (2021).
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
Researchers at the Medical University of South Carolina (MUSC), Ralph H.
Johnson VA Medical Center and elsewhere have reported a link between the complement system and the chronic phase of TBI.
Their results were published online on January 12 in the Journal of Neuroscience, and the results showed that inhibition of complement two months after TBI disrupted neurodegeneration and improved cognitive function.
Johnson VA Medical Center and elsewhere have reported a link between the complement system and the chronic phase of TBI.
Their results were published online on January 12 in the Journal of Neuroscience, and the results showed that inhibition of complement two months after TBI disrupted neurodegeneration and improved cognitive function.
"The vast majority of studies that study different therapies in TBI are done with acute therapy within a few hours after the acute attack.
Our research is of great significance because we will start treatment two months after TBI.
"
Our research is of great significance because we will start treatment two months after TBI.
"
(Image source: style="text-align: justify;">In order to understand the timing of complement and chronic TBI more comprehensively, the author first studied the body's response to the damaged part.
They found that certain brain cells called microglia disrupted synapses characterized by complement.
This process reduces the total number and density of synapses in the brain.
In addition, they reported sustained complement activation for up to three months after a TBI injury, and expanded neuroinflammation throughout the brain area.
This inflammatory response promotes the degeneration of synapses and heralds progressive cognitive decline.
They found that certain brain cells called microglia disrupted synapses characterized by complement.
This process reduces the total number and density of synapses in the brain.
In addition, they reported sustained complement activation for up to three months after a TBI injury, and expanded neuroinflammation throughout the brain area.
This inflammatory response promotes the degeneration of synapses and heralds progressive cognitive decline.
The researchers then studied the therapeutic effects of blocking complement.
They used a complement inhibitor that specifically targets areas of complement activation and brain cell damage.
Inhibition of complement interrupted the decline in brain cell function and reversed mental loss in the task of assessing spatial learning and memory, even if the administration of the inhibitor was postponed to two months after the injury.
They used a complement inhibitor that specifically targets areas of complement activation and brain cell damage.
Inhibition of complement interrupted the decline in brain cell function and reversed mental loss in the task of assessing spatial learning and memory, even if the administration of the inhibitor was postponed to two months after the injury.
The author of the article, Tomlinson, said: "A major advantage of our approach is that we do not systematically inhibit complement activity.
Acute therapy is not a big problem, but long-term treatment of patients with complement inhibitors systematically is not the best choice, because Complement also has other important functions, from host defense to controlling homeostasis and regeneration mechanisms.
"
Acute therapy is not a big problem, but long-term treatment of patients with complement inhibitors systematically is not the best choice, because Complement also has other important functions, from host defense to controlling homeostasis and regeneration mechanisms.
"
So far, treatment research in preclinical models has almost completely focused on the acute treatment of TBI.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
These findings are critical because rehabilitation intervention is the only management strategy available for TBI to improve cognitive and motor function.
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
Source of information: com/news/2021-03-complement-inhibition-reverses-mental-losses.
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
Original source: Ali Alawieh et al, Complement Drives Synaptic Degeneration and Progressive Cognitive Decline in the Chronic Phase after Traumatic Brain Injury, The Journal of Neuroscience (2021).
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
"The vast majority of studies that study different therapies in TBI are done with acute therapy within a few hours after the acute attack.
Our research is of great significance because we will start treatment two months after TBI.
"
Our research is of great significance because we will start treatment two months after TBI.
"
(Image source: style="text-align: justify;">In order to understand the timing of complement and chronic TBI more comprehensively, the author first studied the body's response to the damaged part.
They found that certain brain cells called microglia disrupted synapses characterized by complement.
This process reduces the total number and density of synapses in the brain.
In addition, they reported sustained complement activation for up to three months after a TBI injury, and expanded neuroinflammation throughout the brain area.
This inflammatory response promotes the degeneration of synapses and heralds progressive cognitive decline.
They found that certain brain cells called microglia disrupted synapses characterized by complement.
This process reduces the total number and density of synapses in the brain.
In addition, they reported sustained complement activation for up to three months after a TBI injury, and expanded neuroinflammation throughout the brain area.
This inflammatory response promotes the degeneration of synapses and heralds progressive cognitive decline.
The researchers then studied the therapeutic effects of blocking complement.
They used a complement inhibitor that specifically targets areas of complement activation and brain cell damage.
Inhibition of complement interrupted the decline in brain cell function and reversed mental loss in the task of assessing spatial learning and memory, even if the administration of the inhibitor was postponed to two months after the injury.
They used a complement inhibitor that specifically targets areas of complement activation and brain cell damage.
Inhibition of complement interrupted the decline in brain cell function and reversed mental loss in the task of assessing spatial learning and memory, even if the administration of the inhibitor was postponed to two months after the injury.
The author of the article, Tomlinson, said: "A major advantage of our approach is that we do not systematically inhibit complement activity.
Acute therapy is not a big problem, but long-term treatment of patients with complement inhibitors systematically is not the best choice, because Complement also has other important functions, from host defense to controlling homeostasis and regeneration mechanisms.
"
Acute therapy is not a big problem, but long-term treatment of patients with complement inhibitors systematically is not the best choice, because Complement also has other important functions, from host defense to controlling homeostasis and regeneration mechanisms.
"
So far, treatment research in preclinical models has almost completely focused on the acute treatment of TBI.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
These findings are critical because rehabilitation intervention is the only management strategy available for TBI to improve cognitive and motor function.
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
Source of information: com/news/2021-03-complement-inhibition-reverses-mental-losses.
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
Original source: Ali Alawieh et al, Complement Drives Synaptic Degeneration and Progressive Cognitive Decline in the Chronic Phase after Traumatic Brain Injury, The Journal of Neuroscience (2021).
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
(Image source: style="text-align: justify;">In order to understand the timing of complement and chronic TBI more comprehensively, the author first studied the body's response to the damaged part.
They found that certain brain cells called microglia disrupted synapses characterized by complement.
This process reduces the total number and density of synapses in the brain.
In addition, they reported sustained complement activation for up to three months after a TBI injury, and expanded neuroinflammation throughout the brain area.
This inflammatory response promotes the degeneration of synapses and heralds progressive cognitive decline.
They found that certain brain cells called microglia disrupted synapses characterized by complement.
This process reduces the total number and density of synapses in the brain.
In addition, they reported sustained complement activation for up to three months after a TBI injury, and expanded neuroinflammation throughout the brain area.
This inflammatory response promotes the degeneration of synapses and heralds progressive cognitive decline.
The researchers then studied the therapeutic effects of blocking complement.
They used a complement inhibitor that specifically targets areas of complement activation and brain cell damage.
Inhibition of complement interrupted the decline in brain cell function and reversed mental loss in the task of assessing spatial learning and memory, even if the administration of the inhibitor was postponed to two months after the injury.
They used a complement inhibitor that specifically targets areas of complement activation and brain cell damage.
Inhibition of complement interrupted the decline in brain cell function and reversed mental loss in the task of assessing spatial learning and memory, even if the administration of the inhibitor was postponed to two months after the injury.
The author of the article, Tomlinson, said: "A major advantage of our approach is that we do not systematically inhibit complement activity.
Acute therapy is not a big problem, but long-term treatment of patients with complement inhibitors systematically is not the best choice, because Complement also has other important functions, from host defense to controlling homeostasis and regeneration mechanisms.
"
Acute therapy is not a big problem, but long-term treatment of patients with complement inhibitors systematically is not the best choice, because Complement also has other important functions, from host defense to controlling homeostasis and regeneration mechanisms.
"
So far, treatment research in preclinical models has almost completely focused on the acute treatment of TBI.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
These findings are critical because rehabilitation intervention is the only management strategy available for TBI to improve cognitive and motor function.
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
Source of information: com/news/2021-03-complement-inhibition-reverses-mental-losses.
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
Original source: Ali Alawieh et al, Complement Drives Synaptic Degeneration and Progressive Cognitive Decline in the Chronic Phase after Traumatic Brain Injury, The Journal of Neuroscience (2021).
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
The researchers then studied the therapeutic effects of blocking complement.
They used a complement inhibitor that specifically targets areas of complement activation and brain cell damage.
Inhibition of complement interrupted the decline in brain cell function and reversed mental loss in the task of assessing spatial learning and memory, even if the administration of the inhibitor was postponed to two months after the injury.
They used a complement inhibitor that specifically targets areas of complement activation and brain cell damage.
Inhibition of complement interrupted the decline in brain cell function and reversed mental loss in the task of assessing spatial learning and memory, even if the administration of the inhibitor was postponed to two months after the injury.
The author of the article, Tomlinson, said: "A major advantage of our approach is that we do not systematically inhibit complement activity.
Acute therapy is not a big problem, but long-term treatment of patients with complement inhibitors systematically is not the best choice, because Complement also has other important functions, from host defense to controlling homeostasis and regeneration mechanisms.
"
Acute therapy is not a big problem, but long-term treatment of patients with complement inhibitors systematically is not the best choice, because Complement also has other important functions, from host defense to controlling homeostasis and regeneration mechanisms.
"
So far, treatment research in preclinical models has almost completely focused on the acute treatment of TBI.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
These findings are critical because rehabilitation intervention is the only management strategy available for TBI to improve cognitive and motor function.
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
Source of information: com/news/2021-03-complement-inhibition-reverses-mental-losses.
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
Original source: Ali Alawieh et al, Complement Drives Synaptic Degeneration and Progressive Cognitive Decline in the Chronic Phase after Traumatic Brain Injury, The Journal of Neuroscience (2021).
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
The author of the article, Tomlinson, said: "A major advantage of our approach is that we do not systematically inhibit complement activity.
Acute therapy is not a big problem, but long-term treatment of patients with complement inhibitors systematically is not the best choice, because Complement also has other important functions, from host defense to controlling homeostasis and regeneration mechanisms.
"
Acute therapy is not a big problem, but long-term treatment of patients with complement inhibitors systematically is not the best choice, because Complement also has other important functions, from host defense to controlling homeostasis and regeneration mechanisms.
"
So far, treatment research in preclinical models has almost completely focused on the acute treatment of TBI.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
These findings are critical because rehabilitation intervention is the only management strategy available for TBI to improve cognitive and motor function.
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
Source of information: com/news/2021-03-complement-inhibition-reverses-mental-losses.
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
Original source: Ali Alawieh et al, Complement Drives Synaptic Degeneration and Progressive Cognitive Decline in the Chronic Phase after Traumatic Brain Injury, The Journal of Neuroscience (2021).
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
So far, treatment research in preclinical models has almost completely focused on the acute treatment of TBI.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
Armed with new insights into the pathology of TBI, the Tomlinson team suggested that all stages of injury, including chronic time points, may respond to treatments, especially those that involve complement suppression.
These findings are critical because rehabilitation intervention is the only management strategy available for TBI to improve cognitive and motor function.
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
Source of information: com/news/2021-03-complement-inhibition-reverses-mental-losses.
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
Original source: Ali Alawieh et al, Complement Drives Synaptic Degeneration and Progressive Cognitive Decline in the Chronic Phase after Traumatic Brain Injury, The Journal of Neuroscience (2021).
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
These findings are critical because rehabilitation intervention is the only management strategy available for TBI to improve cognitive and motor function.
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
In addition, accumulated evidence suggests that rehabilitation may speed up recovery, but it will not change long-term results.
(Bioon.
com)
Source of information: com/news/2021-03-complement-inhibition-reverses-mental-losses.
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
Original source: Ali Alawieh et al, Complement Drives Synaptic Degeneration and Progressive Cognitive Decline in the Chronic Phase after Traumatic Brain Injury, The Journal of Neuroscience (2021).
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
Source of information: com/news/2021-03-complement-inhibition-reverses-mental-losses.
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
Source of information: com/news/2021-03-complement-inhibition-reverses-mental-losses. html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
Original source: Ali Alawieh et al, Complement Drives Synaptic Degeneration and Progressive Cognitive Decline in the Chronic Phase after Traumatic Brain Injury, The Journal of Neuroscience (2021).
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
html">Complement inhibition reverses mental losses in preclinical traumatic brain injury models
Original source: Ali Alawieh et al, Complement Drives Synaptic Degeneration and Progressive Cognitive Decline in the Chronic Phase after Traumatic Brain Injury, The Journal of Neuroscience (2021).
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
Original source: Ali Alawieh et al, Complement Drives Synaptic Degeneration and Progressive Cognitive Decline in the Chronic Phase after Traumatic Brain Injury, The Journal of Neuroscience (2021).
DOI: 10.
1523/JNEUROSCI.
1734-20.
2020
Original Source: Complement Drives Synaptic Degeneration and Progressive Cognitive Decline in the Chronic Phase after Traumatic Brain Injury, The Journal of NeuroscienceDOI: 10.
1523/JNEUROSCI.
1734-20.
2020
