Phosphatidylserine-dependent neuroprotective signaling promoted by docosahexaenoic acid

Ask your doctor what this means but I think it means fish oil might be neuroprotective in the immediate aftermath of a stroke. Don't listen to me, I know nuthin.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3383770/

Abstract

Enrichment of polyunsaturated fatty acids, particularly docosahexaenoic acid (DHA, 22:6n–3), in the brain is known to be critical for optimal brain development and function. Mechanisms for DHA’s beneficial effects in the nervous system are not clearly understood at present. DHA is incorporated into the phospholipids in neuronal membranes, which in turn can influence not only the membrane chemical and physical properties but also the cell signaling involved in neuronal survival, proliferation and differentiation. Our studies have indicated that DHA supplementation promotes phosphatidylserine (PS) accumulation and inhibits neuronal cell death under challenged conditions, supporting a notion that DHA is an important neuroprotective agent. This article summarizes our findings on the DHA-mediated membrane-related signaling mechanisms that might explain some of the beneficial effects of DHA, particularly on neuronal survival.

Other sections at the link.

3. DHA-mediated protection of neuronal cell death

We have previously demonstrated that DHA supplementation results in inhibition of neuronal apoptosis induced by serum starvation [15,17] or staurosporine (ST, a general PKC inhibitor) treatment [16] in a PS-dependent manner. Activation of caspase-3, a member of cysteine protease family that produces apoptotic cell death in mammalian cells, was significantly inhibited in cells enriched with DHA in both apoptotic models (Fig. 2A). We found that the PS accumulation by DHA is at least in part responsible for the protective effect of DHA. Enrichment of neuro 2A cells with DPAn–6, which accumulates less PS than with DHA enrichment, produced less protection, while OA enrichment, which does not alter PS levels did not have any effects on neuronal cell death (Figs. 1B, ​,2B).2B). When the DHA- or DPAn–6-induced PS accumulation was reduced by supplementing cells in the absence of serine (Fig. 1B), the protective effect of these fatty acids was significantly diminished in comparison to the cells supplemented with these fatty acids in the presence of serine (Fig. 2B). It is well-established that CGC neurons undergo apoptosis when they are cultured in media containing physiological KCl concentrations (5 mM, low KCl) while depolarizing KCl concentrations (25 mM, high KCl) protects CGC neurons from apoptotic cell death [35]. In this primary neuronal culture model, the protective effect of DHA was also apparent. The DHA-supplemented culture showed significantly less TUNEL (TdT-mediated dUTP-biotin nick end-labeling) positive apoptotic cells and contained reduced level of active caspase-3 (Fig. 2C). The protective effects also appear to correlate with the PS accumulation in this model, as the CGC neurons supplemented with DHA contained higher PS levels in comparison to the non-supplemented neurons (Fig. 1D). Similarly, when DHA and PS levels were lowered in vivo by dietary n–3 fatty acid depletion, the hippocampal neuronal cell death observed in culture was significantly increased, particularly when the trophic factor was removed [17]. These data consistently support the notion that DHA’s anti-apoptotic protective effect is at least in part mediated through PS accumulation.