Mechanisms of damage to dopaminergic neurons by activated astrocytes

Astrocyte-mediated neuroinflammation and neuroprotective mechanisms in the pathogenesis of Parkinson disease. On exposure to inflammatory stimuli, astrocytes become activated A1 phenotype. A1 phenotype astrocytes secrete pro-inflammatory factors, such as interleukin 1 beta (IL-1b), tumor necrosis factor-alpha (TNF-a), and other inflammatory factors, which further induce neuroinflammation and neurotoxicity mechanisms in the human brain, damaging dopaminergic neurons. A1 phenotype astrocytes secrete pro-inflammatory factors, such as IL-1b, TNF-a, and other inflammatory factors. On the other hand, the neuroprotective mechanism of activated A2 phenotype astrocytes against Parkinson disease includes the release of anti-inflammatory cytokines into the brain as well as the upregulation of neuroprotective trophic factors, anti-inflammatory cytokines including transforming growth factor beta (TGF-β), which inhibit persistent neuroinflammation and, thus, protect dopaminergic neurons. Disease occurs when this balance in the organism is disrupted. (Source: Zhang J, Luo L, Long E, Chen L. Neurotoxicity induced by taxane-derived drugs: analysis of the FAERS database 2017-2021. Expert Opin Drug Saf 2023;22[8]:715-24. Creative Commons Attribution 4.0 International [CC BY 4.0] license, creativecommons.org/licenses/by/4.0.)