Just had to shut somebody down at stocktwits who's

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Here's a learning moment for you.

"PTI-125 reportedly tamped down Aβ-induced inflammatory cytokine release by blocking filamin recruitment to toll-like receptor 4."

So Simufilam "tamped down" AB42. AB42 induces CCR5 so lowering AB42 lowers CCR5's inflammatory cytokines but doesn't eliminate it. Leronlimab stops CCR5 inflammatory cytokines in their tracks.

Not only that but FLNa also binds to CCR5 unless of course leronlimab is used.

Once again I run into a drug that effects one small part of the problem while leronlimab addresses many.

leronlimab regulates -

MapK, Erk 1 and 2, Jak 1, 2 and 3, ATP, mTORc1, TNF-a, TNFSF14, IFNy, NF-kb, bradykinin, NETosis, neuropin-1, PI3k, GM-CSF, IL1b, IL-2, IL-4, IL-6, IL-8, IL-10, IL-13, IL-17, CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL11, CCL13, CCL14, CCL16, VEGF, SYK, SHP1, SHP2, PD-1, C5a, CA-2+,CD38, collagen, macrophage differentiation, TGF-b, MMP-1, MMP-9, FLNa

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This will tell you how vital CCR5 is to the inflammatory responses seen in Alzheimer's.

"The CCR5 and CXCR4 receptors have also been found as partners for filamin, though they interact with different repeat structures of the FLNa protein [18]. Additionally, CD4 also interacts with FLNa [18] and CCR5, which then functions as a structural adaptor for CD4 and chemokine receptor clustering in T cells."

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