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Existing studies have shown that astrocytes undergo functional changes in response to diseases and injuries of the central nervous system (CNS), but the underlying mechanisms of these changes and their therapeutic significance are still unclear
In vivo, the genomic deletion of Il1a, Tnf and C1qa can prevent the death of retinal ganglion cells (RGC) after optic nerve compression (ONC) or in the bead occlusion model of glaucoma, and prolong the SOD1G93A model of amyotrophic lateral sclerosis (ALS) The life span of mice
Astrocytes may contribute to the occurrence and development of neurodegenerative diseases Astrocytes may contribute to the occurrence and development of neurodegenerative diseases
Given that astrocytes can regulate the response of the central nervous system to diseases and injuries, it is speculated that astrocytes may actively kill neurons in neurodegenerative diseases
Astrocytes may be able to actively kill neurons in neurodegenerative diseases Astrocytes may be able to actively kill neurons in neurodegenerative diseases
The mechanism by which reactive astrocyte conditioned medium leads to cell death
The mechanism by which reactive astrocyte conditioned medium leads to cell death
The saturated lipids contained in APOE and APOJ lipid particles are the "primordial culprits" that mediate the toxicity induced by astrocytes, not proteins
Taken together, these results indicate a mechanism by which astrocytes kill cells in the central nervous system
Original source:
Original source:Kevin A.
Kevin A.
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