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Editor’s note iNature is China’s largest academic official account.
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us.
iNature traumatic brain injury (TBI) is the largest non-genetic, non-aging-related risk factor for Alzheimer's disease (AD), but its underlying mechanism is not very clear.
On April 13, 2021, Min-Kyoo Shin and others from the University of Cleveland published a research paper entitled "Reducing acetylated tau is neuroprotective in brain injury" in Cell.
The study found that TBI induces tau acetylation (ac-tau).
These sites are also acetylated in the human AD brain.
This is mediated by S-nitrosylation-GAPDH, which simultaneously inactivates Sirtuin1 deacetylase and activates p300/CBP acetyltransferase, thereby increasing neuronal ac-tau.
Subsequent tau positioning errors can lead to neurodegeneration and neurobehavioral impairment, and ac-tau can accumulate in the blood.
Blocking GAPDH S-nitrosylation, inhibiting p300/CBP or stimulating Sirtuin1 can protect mice from neurodegeneration after TBI, neurobehavioral impairment, and accumulation of ac-tau in the blood and brain.
Therefore, Ac-tau is a therapeutic target of TBI and a potential blood biomarker, which may represent the pathological convergence between TBI and AD.
In AD patients with a history of TBI, ac-tau in the brain will further increase; patients with clinically diagnosed TBI who receive p300/CBP Salsalate or diflunisal inhibitors show a lower incidence of AD.
Traumatic head injury (TBI) is usually caused by a motor vehicle crash, fall, contact sports, or beating.
In the United States alone, the annual incidence of TBI is about 3.
5 million, and there are currently about 5 million people suffering from traumatic brain injury (TBI)-related disabilities, and the annual cost is about $80 billion.
At present, the treatment of traumatic brain injury (TBI) focuses on patient stability and symptom relief, and there are no drugs specifically targeting the pathophysiological process of neurodegenerative diseases after brain injury.
Traumatic head injury (TBI) also significantly increases the risk of Alzheimer's disease (AD) in the future.
This indicates a common pathological mechanism, and emerging evidence suggests that S-nitrosylation and acetylation play an important role.
In fact, a recent small autopsy report showed an increase in tau acetylation at lysine (K) 280 in the brains of three AD patients and three chronic traumatic encephalopathy patients; in another study, in another The same elevation of ac-tau at K280 was recorded in the brains of 280 AD patients, 5 patients with cortical basal degeneration, and 5 patients with progressive supranuclear palsy.
In another 12 patients with severe AD, both K274 and K281 showed Tau acetylation.
However, these studies have not determined the driving force or pathological significance of the findings.
The study found that TBI induces tau acetylation (ac-tau), and these sites are also acetylated in the human AD brain.
This is mediated by S-nitrosylation-GAPDH, which simultaneously inactivates Sirtuin1 deacetylase and activates p300/CBP acetyltransferase, thereby increasing neuronal ac-tau.
Subsequent tau positioning errors can lead to neurodegeneration and neurobehavioral impairment, and ac-tau can accumulate in the blood.
Article pattern (picture from Cell) Blocking GAPDH S-nitrosylation, inhibiting p300/CBP or stimulating Sirtuin1 can protect mice from neurodegeneration after TBI, neurobehavioral impairment and ac-tau blood And brain accumulation.
Therefore, Ac-tau is a therapeutic target of TBI and a potential blood biomarker, which may represent the pathological convergence between TBI and AD.
In AD patients with a history of TBI, ac-tau in the brain will further increase; patients with clinically diagnosed TBI who receive p300/CBP Salsalate or diflunisal inhibitors show a lower incidence of AD.
Reference message: #%20
It is jointly created by the doctoral team of Tsinghua University, Harvard University, Chinese Academy of Sciences and other units.
The iNature Talent Official Account is now launched, focusing on talent recruitment, academic progress, scientific research information, interested parties can Long press or scan the QR code below to follow us.
iNature traumatic brain injury (TBI) is the largest non-genetic, non-aging-related risk factor for Alzheimer's disease (AD), but its underlying mechanism is not very clear.
On April 13, 2021, Min-Kyoo Shin and others from the University of Cleveland published a research paper entitled "Reducing acetylated tau is neuroprotective in brain injury" in Cell.
The study found that TBI induces tau acetylation (ac-tau).
These sites are also acetylated in the human AD brain.
This is mediated by S-nitrosylation-GAPDH, which simultaneously inactivates Sirtuin1 deacetylase and activates p300/CBP acetyltransferase, thereby increasing neuronal ac-tau.
Subsequent tau positioning errors can lead to neurodegeneration and neurobehavioral impairment, and ac-tau can accumulate in the blood.
Blocking GAPDH S-nitrosylation, inhibiting p300/CBP or stimulating Sirtuin1 can protect mice from neurodegeneration after TBI, neurobehavioral impairment, and accumulation of ac-tau in the blood and brain.
Therefore, Ac-tau is a therapeutic target of TBI and a potential blood biomarker, which may represent the pathological convergence between TBI and AD.
In AD patients with a history of TBI, ac-tau in the brain will further increase; patients with clinically diagnosed TBI who receive p300/CBP Salsalate or diflunisal inhibitors show a lower incidence of AD.
Traumatic head injury (TBI) is usually caused by a motor vehicle crash, fall, contact sports, or beating.
In the United States alone, the annual incidence of TBI is about 3.
5 million, and there are currently about 5 million people suffering from traumatic brain injury (TBI)-related disabilities, and the annual cost is about $80 billion.
At present, the treatment of traumatic brain injury (TBI) focuses on patient stability and symptom relief, and there are no drugs specifically targeting the pathophysiological process of neurodegenerative diseases after brain injury.
Traumatic head injury (TBI) also significantly increases the risk of Alzheimer's disease (AD) in the future.
This indicates a common pathological mechanism, and emerging evidence suggests that S-nitrosylation and acetylation play an important role.
In fact, a recent small autopsy report showed an increase in tau acetylation at lysine (K) 280 in the brains of three AD patients and three chronic traumatic encephalopathy patients; in another study, in another The same elevation of ac-tau at K280 was recorded in the brains of 280 AD patients, 5 patients with cortical basal degeneration, and 5 patients with progressive supranuclear palsy.
In another 12 patients with severe AD, both K274 and K281 showed Tau acetylation.
However, these studies have not determined the driving force or pathological significance of the findings.
The study found that TBI induces tau acetylation (ac-tau), and these sites are also acetylated in the human AD brain.
This is mediated by S-nitrosylation-GAPDH, which simultaneously inactivates Sirtuin1 deacetylase and activates p300/CBP acetyltransferase, thereby increasing neuronal ac-tau.
Subsequent tau positioning errors can lead to neurodegeneration and neurobehavioral impairment, and ac-tau can accumulate in the blood.
Article pattern (picture from Cell) Blocking GAPDH S-nitrosylation, inhibiting p300/CBP or stimulating Sirtuin1 can protect mice from neurodegeneration after TBI, neurobehavioral impairment and ac-tau blood And brain accumulation.
Therefore, Ac-tau is a therapeutic target of TBI and a potential blood biomarker, which may represent the pathological convergence between TBI and AD.
In AD patients with a history of TBI, ac-tau in the brain will further increase; patients with clinically diagnosed TBI who receive p300/CBP Salsalate or diflunisal inhibitors show a lower incidence of AD.
Reference message: #%20
