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Author | xiao xia editor | Wang Cong typesetting | Alzheimer's disease (AD), commonly known as "Alzheimer's disease", is a serious neurodegenerative disease.
Patients usually suffer from memory loss and learning The main symptoms of weakened ability, accompanied by emotional adjustment disorders and loss of exercise ability, greatly affect the development of individuals, families and society
.
Currently, about 50 million people worldwide suffer from Alzheimer's disease
.
As the average life expectancy of human beings increases and the aging society intensifies, the prevalence of Alzheimer's disease is also rising.
It is estimated that by 2050, Alzheimer's patients will increase to more than 150 million
.
Regrettably, the cause of Alzheimer’s disease is complex, and the scientific community has not yet deciphered the specific mechanism of Alzheimer’s disease.
The mainstream view is that the cause is that the deposition of β-amyloid (Aβ) and Tau protein causes nerves.
Yuan died in large numbers
.
Even international pharmaceutical giants such as Pfizer, Johnson & Johnson, Roche, etc.
are also troubled.
After spending tens of billions of dollars on clinical trials of drugs targeting these two targets, major pharmaceutical companies in the world have not succeeded.
This also makes people feel unsuccessful.
I began to wonder if the direction of Alzheimer's drug research and development was wrong
.
In recent years, a unique type of tau protein-cis-P-tau protein has been discovered, which is the cis-isomer of P-tau protein and is an early driving factor of neurodegeneration caused by traumatic brain injury.
Its role in Alzheimer's disease is unclear
.
On June 2, 2021, the research team led by Lu Kunping and Zhou Xiaozhen of Harvard Medical School published a study titled: Cis P-tau underlies vascular contribution to cognitive impairment and dementia and can be effectively targeted by immunotherapy in mice in the journal Science Translational Medicine Thesis
.
The study discovered a unique type of tau protein, called cis-P-tau protein, which can drive neuronal degeneration
.
In mouse models of vascular dementia and Alzheimer's disease, antibodies targeting the cis-P-tau protein can improve neurodegeneration and memory loss
.
Previous research by the research team has shown that Pin1 enzyme prevents neurodegeneration by converting P-tau from a cis conformation to a trans conformation
.
They found that, unlike the trans structure, cis P-tau disrupted the health of neurons in a process before tau tangles were formed
.
In this study, the research team first detected cis-P-tau in human vascular dementia samples lacking toxic tau tangles, which are a hallmark of Alzheimer’s disease
.
It also caused some changes in gene expression in patients with early Alzheimer's disease
.
Therefore, researchers believe that cis-P-tau can be used as a target for the treatment of vascular dementia or early Alzheimer's disease
.
The anti-cis P-tau antibody was used to treat a mouse model of dementia
.
The drug reversed some of the central nervous system malfunctions, including neuroinflammation and the loss of neurons that protect the myelin sheath
.
Animals treated with antibodies also showed better functional results, such as spatial memory and motor memory
.
The researchers wanted to determine whether the cis-P-tau protein played any role in the neurodegenerative process of Alzheimer's disease, which is marked by the aggregation of tau protein clusters
.
So they used a mouse model carrying the human tau gene
.
In three-month-old mice without tau tangles, the research team found that cis-P-tau was induced and transferred to nerve fibers
.
At this time, treatment of rodents with antibodies can completely prevent learning and memory disorders
.
The antibody also improved symptoms in 13-month-old mice, which had already shown a decline in cognitive abilities, even though the drug did not clear the existing tau protein tangles
.
The research team also performed single-cell gene sequencing analysis
.
The results showed that in the mouse model of vascular dementia, the expression of multiple genes changed, and the cis-P-tau antibody recovered about 85% to 90% of the changes
.
More importantly, injection of purified cis-P-tau in mice induced some of the same genetic changes that also occurred in human patients with early Alzheimer's disease
.
Research on the deposition of tau protein in Alzheimer's disease has suffered many setbacks
.
Last fall, Roche’s anti-tau monoclonal antibody semorinemab failed in an early phase 2 clinical trial for Alzheimer’s disease and failed to improve dementia symptoms or activities of daily living
.
In this study, anti-cis P-tau antibodies can restore the cognitive function of mice without reducing tau tangles, which supports the view that the accumulation of tau is actually not harmful to the nervous system
.
Treatment of neurodegeneration caused by neurovascular injury and traumatic brain injury in Alzheimer's disease through immunotherapy has the potential to target cis-P-tau
.
Compared with other tau drugs, this drug may have several advantages
.
First, it will specifically target the problematic cis-P-tau without affecting the trans-P-tau
.
Second, cis-P-tau antibodies may target early disease drivers before tangles are formed in the brain, rather than pursuing tau accumulation
.
In addition, the drug works in mice without tau mutations, which may be important because many human tau-related diseases are not caused by tau mutations or overexpression
.
Original link: https://stm.
sciencemag.
org/content/13/596/eaaz7615 is open to reprint this article is open to reprint: just leave a message in this article to inform
Patients usually suffer from memory loss and learning The main symptoms of weakened ability, accompanied by emotional adjustment disorders and loss of exercise ability, greatly affect the development of individuals, families and society
.
Currently, about 50 million people worldwide suffer from Alzheimer's disease
.
As the average life expectancy of human beings increases and the aging society intensifies, the prevalence of Alzheimer's disease is also rising.
It is estimated that by 2050, Alzheimer's patients will increase to more than 150 million
.
Regrettably, the cause of Alzheimer’s disease is complex, and the scientific community has not yet deciphered the specific mechanism of Alzheimer’s disease.
The mainstream view is that the cause is that the deposition of β-amyloid (Aβ) and Tau protein causes nerves.
Yuan died in large numbers
.
Even international pharmaceutical giants such as Pfizer, Johnson & Johnson, Roche, etc.
are also troubled.
After spending tens of billions of dollars on clinical trials of drugs targeting these two targets, major pharmaceutical companies in the world have not succeeded.
This also makes people feel unsuccessful.
I began to wonder if the direction of Alzheimer's drug research and development was wrong
.
In recent years, a unique type of tau protein-cis-P-tau protein has been discovered, which is the cis-isomer of P-tau protein and is an early driving factor of neurodegeneration caused by traumatic brain injury.
Its role in Alzheimer's disease is unclear
.
On June 2, 2021, the research team led by Lu Kunping and Zhou Xiaozhen of Harvard Medical School published a study titled: Cis P-tau underlies vascular contribution to cognitive impairment and dementia and can be effectively targeted by immunotherapy in mice in the journal Science Translational Medicine Thesis
.
The study discovered a unique type of tau protein, called cis-P-tau protein, which can drive neuronal degeneration
.
In mouse models of vascular dementia and Alzheimer's disease, antibodies targeting the cis-P-tau protein can improve neurodegeneration and memory loss
.
Previous research by the research team has shown that Pin1 enzyme prevents neurodegeneration by converting P-tau from a cis conformation to a trans conformation
.
They found that, unlike the trans structure, cis P-tau disrupted the health of neurons in a process before tau tangles were formed
.
In this study, the research team first detected cis-P-tau in human vascular dementia samples lacking toxic tau tangles, which are a hallmark of Alzheimer’s disease
.
It also caused some changes in gene expression in patients with early Alzheimer's disease
.
Therefore, researchers believe that cis-P-tau can be used as a target for the treatment of vascular dementia or early Alzheimer's disease
.
The anti-cis P-tau antibody was used to treat a mouse model of dementia
.
The drug reversed some of the central nervous system malfunctions, including neuroinflammation and the loss of neurons that protect the myelin sheath
.
Animals treated with antibodies also showed better functional results, such as spatial memory and motor memory
.
The researchers wanted to determine whether the cis-P-tau protein played any role in the neurodegenerative process of Alzheimer's disease, which is marked by the aggregation of tau protein clusters
.
So they used a mouse model carrying the human tau gene
.
In three-month-old mice without tau tangles, the research team found that cis-P-tau was induced and transferred to nerve fibers
.
At this time, treatment of rodents with antibodies can completely prevent learning and memory disorders
.
The antibody also improved symptoms in 13-month-old mice, which had already shown a decline in cognitive abilities, even though the drug did not clear the existing tau protein tangles
.
The research team also performed single-cell gene sequencing analysis
.
The results showed that in the mouse model of vascular dementia, the expression of multiple genes changed, and the cis-P-tau antibody recovered about 85% to 90% of the changes
.
More importantly, injection of purified cis-P-tau in mice induced some of the same genetic changes that also occurred in human patients with early Alzheimer's disease
.
Research on the deposition of tau protein in Alzheimer's disease has suffered many setbacks
.
Last fall, Roche’s anti-tau monoclonal antibody semorinemab failed in an early phase 2 clinical trial for Alzheimer’s disease and failed to improve dementia symptoms or activities of daily living
.
In this study, anti-cis P-tau antibodies can restore the cognitive function of mice without reducing tau tangles, which supports the view that the accumulation of tau is actually not harmful to the nervous system
.
Treatment of neurodegeneration caused by neurovascular injury and traumatic brain injury in Alzheimer's disease through immunotherapy has the potential to target cis-P-tau
.
Compared with other tau drugs, this drug may have several advantages
.
First, it will specifically target the problematic cis-P-tau without affecting the trans-P-tau
.
Second, cis-P-tau antibodies may target early disease drivers before tangles are formed in the brain, rather than pursuing tau accumulation
.
In addition, the drug works in mice without tau mutations, which may be important because many human tau-related diseases are not caused by tau mutations or overexpression
.
Original link: https://stm.
sciencemag.
org/content/13/596/eaaz7615 is open to reprint this article is open to reprint: just leave a message in this article to inform
