A fatty acid amide activates myeloid cells and improves neurovascular outcomes in retinal degeneration.

Erucamide (22:1 monounsaturated omega-9 fatty acid amide) is highly dysregulated during photoreceptor degeneration in mice and activates retinal myeloid cells to limit vascular and neuronal degeneration.

• Why it matters: Neurovasculoglial cross-talk and neuroimmune signaling that break down the neurovascular unit are central to retinal disease, yet the specific fatty acid amide molecules and mechanisms are unresolved.
• What they did: An unbiased high-resolution metabolomics screen identified erucamide dysregulation in a mouse model of photoreceptor degeneration; in vivo delivery via organosilane-modified porous silicon nanoparticles activated retinal myeloid cells, and TMEM19 was identified as an erucamide binding protein required for activation and neuroprotection.
• The result: Erucamide-driven myeloid activation increased angiogenic and neurotrophic cytokines and limited vascular and neuronal degeneration, supporting a primary fatty acid amide pathway and proposing erucamide/analogs as candidate therapeutics.

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