Thanks to jakeflies and you for posting the article.

From the research paper -

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We found that the microglial-derived CCL-3/-4/-5 bind and activate neuronal CCR5, which in turn promotes mTORC1 activation and disrupts autophagy and aggregate-prone protein clearance.

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Part of the same sequence I proposed for leronlimab acting as a mild antiviral in Covid . "CCR5 blockade of CCL5 disrupts the PI3K/AKT/mTORC1/4E-BP1 pathway dysregulating elF4E. With elF4E disrupted the COVID-19 virus 5' -end cap would be unable to separate it's mRNA and duplicate."

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CCL5-induced CCR5 activation increases mTORC1 activity via PI3K-AKT-TSC2 pathway

Importantly, AKT can promote mTORC1 activity by phosphorylating and inhibiting its well-known suppressor TSC2

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Very interesting. TSC2 is a tumor suppressing gene so yet another way that leronlimab could help in cancer.

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we incubated mouse primary neurons in conditioned media derived from mouse primary microglia previously cultured in basal conditions or activated with lipopolysaccharide (LPS) and interferon gamma (IFNγ). Recently, it has been shown that these factors provoke Alzheimer’s disease-relevant changes in mouse and human induced pluripotent stem cell (iPSC)-derived microglial transcriptomes, suggesting that they phenocopy the microglial activation and the inflammatory response observed in neurodegenerative conditions.

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Lipopolysaccharide induces a very strong immune response including an increase in the CCR5 receptor. IFNy elevates CCR5 and CCR5 then further increases IFNy in a feedback loop.

Meanwhile the FDA has a hold on a drug that can actually help, unlike aduhelm.

https://www.cell.com/neuron/fulltext/S0896-6273(23)00268-4?