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▎The editors of WuXi AppTec's content team forgot where they were and what they wanted to do, lost their way in familiar places, couldn't remember the house number of the house, couldn't recognize the appearance of family members, spoke and read became difficult, and even their temperament changed drastically.
.
.
in China , There are about 10 million elderly people experiencing such pain.
Alzheimer's disease is a progressive cognitive degeneration syndrome caused by brain injury or disease, and the magnitude of this degeneration is much higher than normal aging progress.
"Until now, everyone knows a cancer survivor, but no one knows an Alzheimer's disease survivor.
" "The End of Alzheimer's" wrote in the book.
On April 22, researchers at the Albert Einstein College of Medicine in New York, the United States, announced the design of an experimental drug designed to stimulate a special cell "garbage cleanup" mechanism, which can be used in animal models.
Reversing the main symptoms of Alzheimer’s disease.
The research was published online today in the journal Cell.
This drug-targeted system is called chaperone-mediated autophagy (CMA).
In this system, proteins are combined with molecular chaperones and are transported to the intracellular "junk" called lysosomes.
Treatment station" and then degrade there.
1.
Is damage to CMA related to Alzheimer's disease? The research team first studied the relationship between CMA impairment and Alzheimer's disease.
They genetically engineered mice to lose CMA in the excitatory brain neurons.
This is enough to cause short-term memory loss, impaired walking ability, and other common symptoms that appear in rodent models of Alzheimer's disease.
In addition, the lack of CMA severely disrupts protein homeostasis (the cell's ability to regulate the protein contained in it).
Under normal circumstances, soluble proteins become insoluble, and there is a risk of agglomeration into toxic aggregates.
As people age, the efficiency of CMA becomes lower and lower, thus increasing the risk of unwanted proteins accumulating into insoluble clumps and destroying cells.
Alzheimer’s disease and all other neurodegenerative diseases are characterized by the presence of toxic protein aggregates in the patient’s brain.
The paper reveals the dynamic interaction between CMA and Alzheimer's disease: Alzheimer's disease is related to the loss of CMA in neurons.
▲Cells when CMA is working normally and cells lacking CMA (picture source: reference [3]) 2.
So will early Alzheimer's disease damage CMA function? The research team studied a mouse model of early Alzheimer's disease.
In this model, brain neurons express defective Tau protein.
Abnormal aggregation of tau proteins can form neurofibrillary tangles, which can lead to Alzheimer's disease.
The research team focused on the CMA activity in neurons in the hippocampus, which is an area of the brain that is essential for memory and learning.
They found that compared with control animals, the CMA activity in these neurons was significantly reduced.
The researchers further observed the single-cell RNA sequencing data of brain neurons in patients with Alzheimer's disease and control healthy individuals.
The sequencing data showed the activity level of CMA in the patient's brain tissue.
Sure enough, CMA activity in patients with early Alzheimer's disease is inhibited, and CMA in the brain of patients with advanced Alzheimer's disease is more inhibited.
"When people reach the age of 70 or 80, the activity of CMA usually decreases by about 30% compared to when they are younger.
Most people’s brains can make up for this decline.
But if you add neurodegenerative diseases, it’s normal for brain neurons.
The impact of protein composition can be devastating. Our research shows that CMA deficiency interacts with the pathology of Alzheimer's disease, which greatly accelerates the deterioration of the disease.
"One of the leaders of this research, Professor Ana Maria Cuervo of Einstein College of Medicine, said.
Image source: 123RF3.
A new drug that can remove "junk protein" and reverse symptoms! In CMA, a kind of chaperone is called chaperone The protein binds to damaged or defective proteins in the body’s cells.
These partners transport their cargo to the cell’s lysosomes (membranous organelles filled with enzymes for digestion and recycling of waste).
In order to successfully transfer them When the cargo is delivered to the lysosome, the chaperone protein molecule must first bind to the receptor called LAMP2A on the surface of the
lysosome.
The more LAMP2A receptors on the lysosome, the higher the CMA activity may be.
Researchers have developed a A new drug called CA works by increasing the number of LAMP2A receptors.
▲One of the corresponding authors of this study, Professor Ana Maria Cuervo from the Department of Development and Molecular Biology of Albert Einstein College of Medicine (picture Source: CREDIT Albert Einstein College of Medicine) "The production rate of LAMP2A has not changed in a person's life.
"Professor Cuervo said, "But with age, these receptors degenerate faster.
As a result, there are fewer and fewer available receptors for the delivery of unwanted proteins to lysosomes in the elderly.
CA restores LAMP2A to a youthful level, allowing CMA to clear out Tau protein and other defective proteins, preventing them from forming toxic protein clumps.
"Researchers tested CA in two different mouse models of Alzheimer's disease.
Experimental results show that oral CA for more than 4 to 6 months can improve memory, depression and anxiety, and make the treated mice close to healthy controls.
Group mice.
Not only that, in another group of models, the walking ability of diseased mice was also significantly improved.
In the brain neurons of the two animal models, the drug significantly reduced the levels of Tau protein and other protein clumps compared to untreated animals.
At present, the research team has created a start-up biotechnology company called Selphagy Therapeutics, based on CA to further develop therapies for the treatment of Alzheimer's disease and other neurodegenerative diseases.
Reference: [1] Experimental drug shows potential against Alzheimer's disease.
Retrieved April 22, 2021, from [2] Startup aims to treat Alzheimer's by invigorating neurons' garbage-disposal abilities.
Retrieved April 22, 2021, from system[3] Bourdenx et al.
, (2021).
Chaperone-mediated autophagy prevents collapse of the neuronal metastable proteome.
DOI: https://doi.
org/10.
1016/j.
cell.
2021.
03.
048 Note: This article aims to introduce The progress of medical and health research is not a treatment recommendation.
If you need guidance on treatment plans, please go to a regular hospital for treatment.
.
.
in China , There are about 10 million elderly people experiencing such pain.
Alzheimer's disease is a progressive cognitive degeneration syndrome caused by brain injury or disease, and the magnitude of this degeneration is much higher than normal aging progress.
"Until now, everyone knows a cancer survivor, but no one knows an Alzheimer's disease survivor.
" "The End of Alzheimer's" wrote in the book.
On April 22, researchers at the Albert Einstein College of Medicine in New York, the United States, announced the design of an experimental drug designed to stimulate a special cell "garbage cleanup" mechanism, which can be used in animal models.
Reversing the main symptoms of Alzheimer’s disease.
The research was published online today in the journal Cell.
This drug-targeted system is called chaperone-mediated autophagy (CMA).
In this system, proteins are combined with molecular chaperones and are transported to the intracellular "junk" called lysosomes.
Treatment station" and then degrade there.
1.
Is damage to CMA related to Alzheimer's disease? The research team first studied the relationship between CMA impairment and Alzheimer's disease.
They genetically engineered mice to lose CMA in the excitatory brain neurons.
This is enough to cause short-term memory loss, impaired walking ability, and other common symptoms that appear in rodent models of Alzheimer's disease.
In addition, the lack of CMA severely disrupts protein homeostasis (the cell's ability to regulate the protein contained in it).
Under normal circumstances, soluble proteins become insoluble, and there is a risk of agglomeration into toxic aggregates.
As people age, the efficiency of CMA becomes lower and lower, thus increasing the risk of unwanted proteins accumulating into insoluble clumps and destroying cells.
Alzheimer’s disease and all other neurodegenerative diseases are characterized by the presence of toxic protein aggregates in the patient’s brain.
The paper reveals the dynamic interaction between CMA and Alzheimer's disease: Alzheimer's disease is related to the loss of CMA in neurons.
▲Cells when CMA is working normally and cells lacking CMA (picture source: reference [3]) 2.
So will early Alzheimer's disease damage CMA function? The research team studied a mouse model of early Alzheimer's disease.
In this model, brain neurons express defective Tau protein.
Abnormal aggregation of tau proteins can form neurofibrillary tangles, which can lead to Alzheimer's disease.
The research team focused on the CMA activity in neurons in the hippocampus, which is an area of the brain that is essential for memory and learning.
They found that compared with control animals, the CMA activity in these neurons was significantly reduced.
The researchers further observed the single-cell RNA sequencing data of brain neurons in patients with Alzheimer's disease and control healthy individuals.
The sequencing data showed the activity level of CMA in the patient's brain tissue.
Sure enough, CMA activity in patients with early Alzheimer's disease is inhibited, and CMA in the brain of patients with advanced Alzheimer's disease is more inhibited.
"When people reach the age of 70 or 80, the activity of CMA usually decreases by about 30% compared to when they are younger.
Most people’s brains can make up for this decline.
But if you add neurodegenerative diseases, it’s normal for brain neurons.
The impact of protein composition can be devastating. Our research shows that CMA deficiency interacts with the pathology of Alzheimer's disease, which greatly accelerates the deterioration of the disease.
"One of the leaders of this research, Professor Ana Maria Cuervo of Einstein College of Medicine, said.
Image source: 123RF3.
A new drug that can remove "junk protein" and reverse symptoms! In CMA, a kind of chaperone is called chaperone The protein binds to damaged or defective proteins in the body’s cells.
These partners transport their cargo to the cell’s lysosomes (membranous organelles filled with enzymes for digestion and recycling of waste).
In order to successfully transfer them When the cargo is delivered to the lysosome, the chaperone protein molecule must first bind to the receptor called LAMP2A on the surface of the
lysosome.
The more LAMP2A receptors on the lysosome, the higher the CMA activity may be.
Researchers have developed a A new drug called CA works by increasing the number of LAMP2A receptors.
▲One of the corresponding authors of this study, Professor Ana Maria Cuervo from the Department of Development and Molecular Biology of Albert Einstein College of Medicine (picture Source: CREDIT Albert Einstein College of Medicine) "The production rate of LAMP2A has not changed in a person's life.
"Professor Cuervo said, "But with age, these receptors degenerate faster.
As a result, there are fewer and fewer available receptors for the delivery of unwanted proteins to lysosomes in the elderly.
CA restores LAMP2A to a youthful level, allowing CMA to clear out Tau protein and other defective proteins, preventing them from forming toxic protein clumps.
"Researchers tested CA in two different mouse models of Alzheimer's disease.
Experimental results show that oral CA for more than 4 to 6 months can improve memory, depression and anxiety, and make the treated mice close to healthy controls.
Group mice.
Not only that, in another group of models, the walking ability of diseased mice was also significantly improved.
In the brain neurons of the two animal models, the drug significantly reduced the levels of Tau protein and other protein clumps compared to untreated animals.
At present, the research team has created a start-up biotechnology company called Selphagy Therapeutics, based on CA to further develop therapies for the treatment of Alzheimer's disease and other neurodegenerative diseases.
Reference: [1] Experimental drug shows potential against Alzheimer's disease.
Retrieved April 22, 2021, from [2] Startup aims to treat Alzheimer's by invigorating neurons' garbage-disposal abilities.
Retrieved April 22, 2021, from system[3] Bourdenx et al.
, (2021).
Chaperone-mediated autophagy prevents collapse of the neuronal metastable proteome.
DOI: https://doi.
org/10.
1016/j.
cell.
2021.
03.
048 Note: This article aims to introduce The progress of medical and health research is not a treatment recommendation.
If you need guidance on treatment plans, please go to a regular hospital for treatment.
