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- W4382011926 abstract "In the prodromal phase of neurodegenerative diseases, microglia switch to an activated state resulting in increased secretion of pro-inflammatory factors. We reported that C – C chemokine ligand 3 (CCL3), C – C chemokine ligand 4 (CCL4) and C – C chemokine ligand 5 (CCL5) contained in the secretome of activated microglia inhibit neuronal autophagy via a non-cell autonomous mechanism. These chemokines bind and activate neuronal C – C chemokine receptor type 5 (CCR5), which, in turn, promotes phosphoinositide 3-kinase (PI3K) – protein kinase B (PKB, or AKT) – mammalian target of rapamycin complex 1 (mTORC1) pathway activation, which inhibits autophagy, thus causing the accumulation of aggregate-prone proteins in the cytoplasm of neurons. The levels of CCR5 and its chemokine ligands are increased in the brains of pre-manifesting Huntington disease (HD) and tauopathy mouse models. CCR5 accumulation might be due to a self-amplifying mechanism, since CCR5 is a substrate of autophagy and CCL5-CCR5-mediated autophagy inhibition impairs CCR5 degradation. Furthermore, pharmacological, or genetic inhibition of CCR5 rescues mTORC1-autophagy dysfunction and improves neurodegeneration in HD and tauopathy mouse models, suggesting that CCR5 hyperactivation is a pathogenic signal driving the progression of these diseases." @default.
- W4382011926 created "2023-06-27" @default.
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- W4382011926 date "2023-06-26" @default.
- W4382011926 modified "2023-10-14" @default.
- W4382011926 title "Microglial cytokines poison neuronal autophagy via CCR5, a druggable target" @default.
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- W4382011926 doi "https://doi.org/10.1080/15548627.2023.2221921" @default.
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