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Unsaturated lipids originating from tauopathy iPSC neurons and transferred to microglia have the potential to cause LD accumulation, potentially by inhibition of neuronal AMPK signaling

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This flexibility represents both a survival advantage and a therapeutic challenge [20, 21]

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Gastrointestinal effects dominate the tolerability picture Across the Phase 2 obesity, MASH, and diabetes trials, the most consistent finding is a high rate of gastrointestinal adverse events nausea, vomiting, and diarrhea substantially more frequent than placebo

We reexamined this data to look specifically at genes known to be involved in lipogenesis and fatty acid biosynthesis