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Deepak Jha's avatar

Good piece here! Fully agree with the reversal issue vs. slow progression of neurodegeneration.

A key challenge seems to be when to target the glial cells too. Too early/ too late? TREM2 is a good example; too much agonism shuts down downstream signaling (desensitization).

Not to mention, which biomarkers to think about for neuroinflammation or how to consider (or if?) oligodendrocytes.

See recent papers & reviews from Li Huei Tsai et. al for impact of oligos.

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Lois Eure's avatar

This is a cut and paste from another article. Thoughts?

Check this out…

For me and Al:

“4.1.1 Bezisterim (NE3107): A Novel Anti-Neuroinflammatory Agent

A leading example of a novel, purpose-built therapeutic is bezisterim (also known as NE3107).80 Bezisterim is an orally bioavailable, small-molecule drug that can cross the blood-brain barrier, a crucial property for treating CNS conditions.82 It functions as an anti-inflammatory insulin-sensitizer with a novel mechanism of action that involves the selective modulation of the transcription factor Nuclear Factor kappa B (NF−κB) activation, a master regulator of inflammation.81 By binding to the extracellular signal-regulated kinase (ERK), bezisterim inhibits inflammatory signaling and reduces the production of key cytokines like TNF−α, without disrupting the homeostatic functions of these pathways.82”

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