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▎Editor of WuXi AppTec's content team.
Alzheimer's disease is the most prevalent neurodegenerative disease in the world.
Patients show declining cognitive ability, and in their brains, beta amyloid protein accumulates between cells into plaques It is considered to be a typical pathological feature.
▲This study helps us understand the role of different amyloid deposits (picture source: NIH Image Gallery from Bethesda, Maryland, USA / Public domain) For many years, people think that amyloid plaques are caused by Alzheimer's disease The reason is that many scientific studies have also invested in how to remove these toxic plaques in an attempt to reverse the disease.
However, for more than a decade, multiple clinical trials have ended in failure, which also makes people doubt the specific role of amyloid plaques.
Recently, a scientific research team from the Salk Institute published a paper in Nature Immunology, a sub-issue of Nature, and put forward a new view on the "toxicity" of a type of amyloid plaque.
They found that the production of such protein plaques is to protect brain cells, so the treatment of removing protein plaques may bring about more harm than good consequences.
There are many different forms of amyloid plaques.
Among them, "loose" and "dense-core" are the most common, and both are generally considered to be caused by overproduction of amyloid precursor protein (APP).
) And formed spontaneously.
But in this study, scientists have put forward new views on amyloid plaques characterized by "dense nuclei".
"We found that such dense nuclear plaques are not formed spontaneously.
In fact, we believe that they are established by microglia and are a protective mechanism.
" Professor Greg Lemke, who was in charge of this research, pointed out.
Microglia are immune cells in the brain.
The traditional view is that these cells should "eat" protein deposits and inhibit the formation of plaques.
In Professor Lemke's previous research on microglia, they found that after the death of brain cells, some of the lipid molecules inside the cells would turn out and signal "I'm dead, eat me".
Microglial cells recognize the relevant signals through the surface protein TAM receptor, and then swallow these dead cells.
Following this discovery, the team noticed that not only dead cells, but amyloid plaques that are prevalent in Alzheimer's disease also send out the same "eat me" signal.
Using a mouse model, researchers have demonstrated for the first time through experiments that microglia equipped with TAM receptors will indeed recognize and engulf amyloid plaques based on these signals.
▲In the brains of Alzheimer's disease model mice, microglia (white) lacking TAM receptors were observed to surround dense nucleoprotein plaques (red) (picture source: reference [2]; Credit: Salk Institute) further used real-time imaging technology to track dense nuclear protein plaques, and the researchers found a result that surprised them: when microglia eats a loose-shaped plaque, it will eat the beta amyloid.
It is transferred to a highly acidic organelle and converted into dense aggregates and then discharged to form dense nucleoprotein plaques.
In this way, microglia can clear the debris between the cells as a benign compensation for the response to neuroinflammatory and neurodegeneration.
"From our research results, when there are few dense nuclear plaques, it seems to be more harmful to nerve cells.
" First author Dr.
Huang Youtong explained, "When there are more loose plaques, we see a lot of nutrients.
Bad neurites, which is a sign of neuronal damage. "▲Professor Greg Lemke, the corresponding author of this study, and Dr.
Youtong Huang, the first author (picture source: References[2]; Credit: Salk Institute), Professor Lemke added: "The experiment to eliminate dense nuclear protein plaques has relatively failed.
Presenting these results refutes the idea that beta amyloid is harmful to the brain.
But we believe that beta amyloid is still harmful, but you have to distinguish whether dense nuclear plaques are harmful.
"Based on this discovery, the research team has proposed a new direction for the treatment of Alzheimer's disease, such as increasing the expression of TAM receptors on microglia, thereby increasing the recognition of loose plaques and accelerating dense nuclear The formation of plaques.
The
research team believes that finding new therapies will
definitely end the failure of clinical trials of Alzheimer’s disease drugs.
Reference [1] Youtong Huang et al.
, (2021) Microglia use TAM receptors to detect and engulf amyloid β plaques.
Nature Immunology DOI: 10.
1038/s41590-021-00913-5[2] In surprising twist, some Alzheimer's plaques may be protective, not destructive Retrieved Apr.
19, 2021 from -release/in-surprising-twist-some-alzheimers-plaques-may-be-protective-not-destructive/
Alzheimer's disease is the most prevalent neurodegenerative disease in the world.
Patients show declining cognitive ability, and in their brains, beta amyloid protein accumulates between cells into plaques It is considered to be a typical pathological feature.
▲This study helps us understand the role of different amyloid deposits (picture source: NIH Image Gallery from Bethesda, Maryland, USA / Public domain) For many years, people think that amyloid plaques are caused by Alzheimer's disease The reason is that many scientific studies have also invested in how to remove these toxic plaques in an attempt to reverse the disease.
However, for more than a decade, multiple clinical trials have ended in failure, which also makes people doubt the specific role of amyloid plaques.
Recently, a scientific research team from the Salk Institute published a paper in Nature Immunology, a sub-issue of Nature, and put forward a new view on the "toxicity" of a type of amyloid plaque.
They found that the production of such protein plaques is to protect brain cells, so the treatment of removing protein plaques may bring about more harm than good consequences.
There are many different forms of amyloid plaques.
Among them, "loose" and "dense-core" are the most common, and both are generally considered to be caused by overproduction of amyloid precursor protein (APP).
) And formed spontaneously.
But in this study, scientists have put forward new views on amyloid plaques characterized by "dense nuclei".
"We found that such dense nuclear plaques are not formed spontaneously.
In fact, we believe that they are established by microglia and are a protective mechanism.
" Professor Greg Lemke, who was in charge of this research, pointed out.
Microglia are immune cells in the brain.
The traditional view is that these cells should "eat" protein deposits and inhibit the formation of plaques.
In Professor Lemke's previous research on microglia, they found that after the death of brain cells, some of the lipid molecules inside the cells would turn out and signal "I'm dead, eat me".
Microglial cells recognize the relevant signals through the surface protein TAM receptor, and then swallow these dead cells.
Following this discovery, the team noticed that not only dead cells, but amyloid plaques that are prevalent in Alzheimer's disease also send out the same "eat me" signal.
Using a mouse model, researchers have demonstrated for the first time through experiments that microglia equipped with TAM receptors will indeed recognize and engulf amyloid plaques based on these signals.
▲In the brains of Alzheimer's disease model mice, microglia (white) lacking TAM receptors were observed to surround dense nucleoprotein plaques (red) (picture source: reference [2]; Credit: Salk Institute) further used real-time imaging technology to track dense nuclear protein plaques, and the researchers found a result that surprised them: when microglia eats a loose-shaped plaque, it will eat the beta amyloid.
It is transferred to a highly acidic organelle and converted into dense aggregates and then discharged to form dense nucleoprotein plaques.
In this way, microglia can clear the debris between the cells as a benign compensation for the response to neuroinflammatory and neurodegeneration.
"From our research results, when there are few dense nuclear plaques, it seems to be more harmful to nerve cells.
" First author Dr.
Huang Youtong explained, "When there are more loose plaques, we see a lot of nutrients.
Bad neurites, which is a sign of neuronal damage. "▲Professor Greg Lemke, the corresponding author of this study, and Dr.
Youtong Huang, the first author (picture source: References[2]; Credit: Salk Institute), Professor Lemke added: "The experiment to eliminate dense nuclear protein plaques has relatively failed.
Presenting these results refutes the idea that beta amyloid is harmful to the brain.
But we believe that beta amyloid is still harmful, but you have to distinguish whether dense nuclear plaques are harmful.
"Based on this discovery, the research team has proposed a new direction for the treatment of Alzheimer's disease, such as increasing the expression of TAM receptors on microglia, thereby increasing the recognition of loose plaques and accelerating dense nuclear The formation of plaques.
The
research team believes that finding new therapies will
definitely end the failure of clinical trials of Alzheimer’s disease drugs.
Reference [1] Youtong Huang et al.
, (2021) Microglia use TAM receptors to detect and engulf amyloid β plaques.
Nature Immunology DOI: 10.
1038/s41590-021-00913-5[2] In surprising twist, some Alzheimer's plaques may be protective, not destructive Retrieved Apr.
19, 2021 from -release/in-surprising-twist-some-alzheimers-plaques-may-be-protective-not-destructive/
