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Under normal circumstances, astrocytes and microglia maintain neuronal functions by removing debris, recycling neurotransmitter molecules, and supporting cross-synaptic communication
.
Astrocytes and microglia each regulate each other's functions through secretion factors, and this entanglement of glial cells is mostly completed through molecular signals
.
However, in the brains of patients with AD (Alzheimer's disease), astrocytes and microglia are widely activated, secrete inflammatory factors and gather around Aβ protein plaques to play a protective role
.
IL-3 is a multifunctional cytokine, which is closely related to the risk of AD and the severity of symptoms
.
Unexpectedly, this cytokine is actually the key molecule of "glial cell entanglement
.
"
On July 14, 2021, Filip K.
Swirski's research team at Massachusetts General Hospital, Harvard Medical School revealed that IL-3 can act as astrocytes to regulate microglia to play a key regulatory molecule for clearing Aβ protein plaques
.
IL-3 plays a protective role in AD disease.
Researchers crossed IL-3 knockout mice with AD model mice (5xFAD mice).
The Aβ protein plaque deposition in the cortical brain area increased, and the short-term and long-term spatial memory functions were both Damage, indicating that IL-3 may play a protective role in AD model mice
.
Is there a difference between IL-3 in normal mice and AD model mice? They further found that the concentration of IL-3 in the plasma and cerebrospinal fluid (CSF) of normal mice was not different from that of 5xFAD mice, and the concentration of IL-3 in the brains of AD patients was comparable to that of healthy adults
.
But the IL-3 concentration in cerebrospinal fluid is about four times that in plasma
.
Where does the large amount of IL-3 in the brain come from? The researchers used flow cytometry to trace the source and found that astrocytes are the main source of IL-3, and microglia rarely secrete IL-3
.
Further immunofluorescence experiments also found that IL-3 was co-labeled with astrocytes in a large amount, and it was widely distributed in multiple brain areas such as the cortex, hippocampus, and hypothalamus
.
Interestingly, IL-3Rα, the receptor for IL-3, is expressed on microglia
.
Normal 8-month-old mice IL-3Rα-positive microglia account for about 8% of the total number of microglia, but this proportion is as high as 50% in 5xFAD mice of the same age
.
Correspondingly, the expression of IL-3Rα in the cortex of AD patients also increased significantly
.
These results indicate that IL-3Rα, which is abnormally expressed by microglia, may be the biggest "handle" subject to astrocytes
.
The researchers found that after all IL-3 was knocked out, 5xFAD mice's originally activated microglia turned into a resting state, and the ability of microglia to migrate to Aβ protein was also weakened
.
When IL-3 on astrocytes is specifically knocked out or IL-3Rα on microglia is knocked out, Aβ plaques increase while microglia also undergo the above changes
.
These results indicate that IL-3 plays a protective role in the course of AD disease through microglia
.
They injected IL-3 into the cortex of 5xFAD mice to promote the accumulation of microglia around Aβ plaques and inhibit the further formation of plaques
.
One month after continuous injection of IL-3 into the lateral ventricle, the size and number of Aβ plaques and the level of soluble Aβ were significantly reduced, and short-term memory was improved.
.
In summary, this paper found that IL-3 secreted by astrocytes can remodel microglia to improve the pathological process of AD through its receptor IL-3Rα
.
[References] 1.
https://doi.
org/10.
1038/s41586-021-03734-62.
https://doi.
org/10.
1038/d41586-021-01870-7
Under normal circumstances, astrocytes and microglia maintain neuronal functions by removing debris, recycling neurotransmitter molecules, and supporting cross-synaptic communication
.
Astrocytes and microglia each regulate each other's functions through secretion factors, and this entanglement of glial cells is mostly completed through molecular signals
.
However, in the brains of patients with AD (Alzheimer's disease), astrocytes and microglia are widely activated, secrete inflammatory factors and gather around Aβ protein plaques to play a protective role
.
IL-3 is a multifunctional cytokine, which is closely related to the risk of AD and the severity of symptoms
.
Unexpectedly, this cytokine is actually the key molecule of "glial cell entanglement
.
"
On July 14, 2021, Filip K.
Swirski's research team at Massachusetts General Hospital, Harvard Medical School revealed that IL-3 can act as astrocytes to regulate microglia to play a key regulatory molecule for clearing Aβ protein plaques
.
IL-3 plays a protective role in AD disease.
Researchers crossed IL-3 knockout mice with AD model mice (5xFAD mice).
The Aβ protein plaque deposition in the cortical brain area increased, and the short-term and long-term spatial memory functions were both Damage, indicating that IL-3 may play a protective role in AD model mice
.
Is there a difference between IL-3 in normal mice and AD model mice? They further found that the concentration of IL-3 in the plasma and cerebrospinal fluid (CSF) of normal mice was not different from that of 5xFAD mice, and the concentration of IL-3 in the brains of AD patients was comparable to that of healthy adults
.
But the IL-3 concentration in cerebrospinal fluid is about four times that in plasma
.
Where does the large amount of IL-3 in the brain come from? The researchers used flow cytometry to trace the source and found that astrocytes are the main source of IL-3, and microglia rarely secrete IL-3
.
Further immunofluorescence experiments also found that IL-3 was co-labeled with astrocytes in a large amount, and it was widely distributed in multiple brain areas such as the cortex, hippocampus, and hypothalamus
.
Interestingly, IL-3Rα, the receptor for IL-3, is expressed on microglia
.
Normal 8-month-old mice IL-3Rα-positive microglia account for about 8% of the total number of microglia, but this proportion is as high as 50% in 5xFAD mice of the same age
.
Correspondingly, the expression of IL-3Rα in the cortex of AD patients also increased significantly
.
These results indicate that IL-3Rα, which is abnormally expressed by microglia, may be the biggest "handle" subject to astrocytes
.
The researchers found that after all IL-3 was knocked out, 5xFAD mice's originally activated microglia turned into a resting state, and the ability of microglia to migrate to Aβ protein was also weakened
.
When IL-3 on astrocytes is specifically knocked out or IL-3Rα on microglia is knocked out, Aβ plaques increase while microglia also undergo the above changes
.
These results indicate that IL-3 plays a protective role in the course of AD disease through microglia
.
They injected IL-3 into the cortex of 5xFAD mice to promote the accumulation of microglia around Aβ plaques and inhibit the further formation of plaques
.
One month after continuous injection of IL-3 into the lateral ventricle, the size and number of Aβ plaques and the level of soluble Aβ were significantly reduced, and short-term memory was improved.
.
In summary, this paper found that IL-3 secreted by astrocytes can remodel microglia to improve the pathological process of AD through its receptor IL-3Rα
.
[References] 1.
https://doi.
org/10.
1038/s41586-021-03734-62.
https://doi.
org/10.
1038/d41586-021-01870-7
