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Written | xiao xia editor | Wang Duoyu typesetting | Alzheimer's disease, commonly known as Alzheimer's disease, is a progressive neurological dementia that affects thinking, orientation and memory, leading to impaired cognition and behavior.
There are 50 million patients
.
The pathological features of Alzheimer's disease are the accumulation of beta amyloid (Aβ) in neuritic plaques and the appearance of neurofibrillary tangles (NFT) composed of hyperphosphorylated tau protein (tau)
.
In recent years, 65% of clinical trials have used Aβ as a drug target
.
However, these trials are rarely successful, which means that the Alzheimer's treatment targets previously studied may not be correct
.
In addition, the currently approved treatments for Alzheimer's disease treat the symptoms but not the root cause, and cannot stop the progression of the disease at all
.
Therefore, there is an urgent need to develop new methods and drugs
.
More and more evidence supports that Alzheimer's disease may be mediated by vascular dysfunction
.
Studies on mouse models of Alzheimer’s disease and postmortem studies on human brain tissue have shown that cerebral angiogenesis can cause damage to the blood-brain barrier
.
This barrier, mainly composed of blood vessels, is believed to protect the brain from infection, because foreign molecules cannot easily pass through it
.
However, the disease mechanism mediated by angiogenesis has not yet been fully elucidated
.
Recently, the research team of the University of British Columbia in Canada published a research paper titled: Reversing pathology in a preclinical model of Alzheimer's disease by hacking cerebrovascular neoangiogenesis with advanced cancer therapeutics in the sub-Journal EBioMedicine of The Lancet
.
The study used the anticancer drug Axitinib (a small molecule tyrosine kinase inhibitor that targets the vascular endothelial growth factor receptor) to target the pro-angiogenic pathway of Alzheimer's disease, significantly reducing cerebral angiogenesis , Restored the integrity of the blood-brain barrier, reduced β-amyloid protein deposition, and effectively restored the memory and cognitive abilities of Alzheimer's disease mice
.
Therefore, the use of anti-cancer drugs to regulate cerebral angiogenesis, rather than directly targeting amyloid, may provide effective treatment for Alzheimer's disease and related cerebrovascular diseases
.
The Tg2576 transgenic mouse is a classic preclinical model that mimics human Alzheimer's disease
.
The ultimate goal of treatment for patients with Alzheimer's disease is to restore normal cognition and behavior
.
Therefore, the research team used several different behavioral tests to evaluate the effect of Axitinib on Tg mice
.
Untreated Tg mice performed poorly in these tests, while treated Tg mice performed similarly to WT mice, suggesting that axitinib treatment restored the behavior of Tg mice
.
Next, the research team executed the mice and evaluated their brains for angiogenesis
.
They found that compared with untreated Tg mice, the new angiogenesis markers CD105 and Aβ were significantly reduced in mice treated with axitinib, while the tight junction protein ZO1 was significantly increased.
.
Shows that Axitinib treatment alleviates cerebrovascular disease
.
In healthy animals, the physical seal of the blood-brain barrier is mainly maintained by the complete and continuous arrangement of tight junction proteins ZO1, claudin, occludein, and other components of neurovascular units
.
Their changes can lead to the destruction of the tight junctions between endothelial cells, resulting in increased barrier permeability, leading to unimpeded entry of toxic blood components into the brain, thereby promoting the pathology of Alzheimer's disease
.
The research team observed that Tg mice treated with Axitinib showed a lower percentage of tight junction destruction, restoring the integrity of the blood-brain barrier in Tg mice, which is similar to the phenomenon observed in WT
.
In summary, this work has discovered the excellent efficacy of the anti-cancer drug Axitinib on Alzheimer's disease.
Axitinib is an anti-angiogenic drug.
Its success reminds us one point-to transform our thinking : The pharmacological target of Alzheimer's disease should be aimed at the angiogenesis mechanism, rather than directly targeting amyloid
.
Link to the paper: https:// is open for reprinting, welcome to forward to Moments and WeChat groups
There are 50 million patients
.
The pathological features of Alzheimer's disease are the accumulation of beta amyloid (Aβ) in neuritic plaques and the appearance of neurofibrillary tangles (NFT) composed of hyperphosphorylated tau protein (tau)
.
In recent years, 65% of clinical trials have used Aβ as a drug target
.
However, these trials are rarely successful, which means that the Alzheimer's treatment targets previously studied may not be correct
.
In addition, the currently approved treatments for Alzheimer's disease treat the symptoms but not the root cause, and cannot stop the progression of the disease at all
.
Therefore, there is an urgent need to develop new methods and drugs
.
More and more evidence supports that Alzheimer's disease may be mediated by vascular dysfunction
.
Studies on mouse models of Alzheimer’s disease and postmortem studies on human brain tissue have shown that cerebral angiogenesis can cause damage to the blood-brain barrier
.
This barrier, mainly composed of blood vessels, is believed to protect the brain from infection, because foreign molecules cannot easily pass through it
.
However, the disease mechanism mediated by angiogenesis has not yet been fully elucidated
.
Recently, the research team of the University of British Columbia in Canada published a research paper titled: Reversing pathology in a preclinical model of Alzheimer's disease by hacking cerebrovascular neoangiogenesis with advanced cancer therapeutics in the sub-Journal EBioMedicine of The Lancet
.
The study used the anticancer drug Axitinib (a small molecule tyrosine kinase inhibitor that targets the vascular endothelial growth factor receptor) to target the pro-angiogenic pathway of Alzheimer's disease, significantly reducing cerebral angiogenesis , Restored the integrity of the blood-brain barrier, reduced β-amyloid protein deposition, and effectively restored the memory and cognitive abilities of Alzheimer's disease mice
.
Therefore, the use of anti-cancer drugs to regulate cerebral angiogenesis, rather than directly targeting amyloid, may provide effective treatment for Alzheimer's disease and related cerebrovascular diseases
.
The Tg2576 transgenic mouse is a classic preclinical model that mimics human Alzheimer's disease
.
The ultimate goal of treatment for patients with Alzheimer's disease is to restore normal cognition and behavior
.
Therefore, the research team used several different behavioral tests to evaluate the effect of Axitinib on Tg mice
.
Untreated Tg mice performed poorly in these tests, while treated Tg mice performed similarly to WT mice, suggesting that axitinib treatment restored the behavior of Tg mice
.
Next, the research team executed the mice and evaluated their brains for angiogenesis
.
They found that compared with untreated Tg mice, the new angiogenesis markers CD105 and Aβ were significantly reduced in mice treated with axitinib, while the tight junction protein ZO1 was significantly increased.
.
Shows that Axitinib treatment alleviates cerebrovascular disease
.
In healthy animals, the physical seal of the blood-brain barrier is mainly maintained by the complete and continuous arrangement of tight junction proteins ZO1, claudin, occludein, and other components of neurovascular units
.
Their changes can lead to the destruction of the tight junctions between endothelial cells, resulting in increased barrier permeability, leading to unimpeded entry of toxic blood components into the brain, thereby promoting the pathology of Alzheimer's disease
.
The research team observed that Tg mice treated with Axitinib showed a lower percentage of tight junction destruction, restoring the integrity of the blood-brain barrier in Tg mice, which is similar to the phenomenon observed in WT
.
In summary, this work has discovered the excellent efficacy of the anti-cancer drug Axitinib on Alzheimer's disease.
Axitinib is an anti-angiogenic drug.
Its success reminds us one point-to transform our thinking : The pharmacological target of Alzheimer's disease should be aimed at the angiogenesis mechanism, rather than directly targeting amyloid
.
Link to the paper: https:// is open for reprinting, welcome to forward to Moments and WeChat groups
