Short answer: partly yes. The brain benefits of omega-3s aren’t just “more fat in membranes,” they’re heavily driven by enzymatic pro-resolution signals made from those fats: the specialized pro-resolving mediators (SPMs) like resolvins, protectins (notably neuroprotectin D1), and maresins. These flip microglia and astroglia out of chronic alarm mode, stabilize synapses, and promote debris clearance and tissue repair. That’s a different biochemical universe from the random, non-enzymatic lipid peroxidation people worry about. 
What that means in practice
• EPA/DHA are converted by lipoxygenases and CYP enzymes into SPMs in the CNS; the brain can make these locally, and several SPMs (or their stable analogs) work through defined GPCRs (e.g., RvE1→CMKLR1, RvD1→ALX/FPR2, NPD1→GPR37) to dampen neuroinflammation and protect circuits. You’ll see this across models of pain, stroke, trauma, and neurodegeneration. 
• Human and animal work suggests SPMs can act within the brain and are reduced in neurodegenerative states; adding back SPMs or boosting their production improves microglial phagocytosis and resolution. Translation to routine clinical dosing is ongoing, but the direction of evidence is consistent. 
About the “oxidized PUFA load” worry
Yes, highly unsaturated chains are easy targets for peroxidation, especially if your fish oil is stale. But in vivo data are not uniformly grim. RCTs with deliberately oxidized fish oil didn’t show a rise in systemic oxidative-stress markers, and meta-analyses often find omega-3 supplementation lowers malondialdehyde and boosts endogenous antioxidant capacity. Translation: whether the scale tips toward harmful non-enzymatic peroxidation or helpful enzymatic SPM production depends on dose, oil quality, redox status, and co-nutrients, not just on the double bonds existing. 
Other omega-3 brain pathways that aren’t “resolvins”
• Substrate competition with arachidonic-acid eicosanoids (less pro-inflammatory signaling).
• Membrane biophysics and ion-channel modulation that affect synaptic function.
• DHA-derived synaptamide (N-docosahexaenoylethanolamide) acting at GPR110 to promote neurogenesis and anti-inflammatory programs. These mechanisms coexist with SPMs and don’t rely on making more oxidized junk. 
How to bias the system toward “resolution > oxidation”
• Use fresh, well-stored omega-3s with verified low peroxide/anisidine values; rancid oil stacks the deck the wrong way.
• Take with meals and adequate antioxidants (dietary vitamin E, polyphenols).
• Prioritize DHA for CNS-specific aims; EPA remains valuable for systemic inflammatory tone.
• Consider that direct SPM formulations and stable SPM analogs are being explored when you need resolution signaling without large fatty-acid loads. 
Bottom line: resolvins, protectins, and maresins are a major reason omega-3s “work” in the brain, and their benefits can outweigh the peroxidation risk when you’re using quality sources and sane dosing. The trick is nudging biochemistry toward enzymatic resolution rather than letting your supplements turn into a fryer oil cosplay.