I've done work in neuroregeneration, and it looks like these lipids appear in neurogenic regions of the mouse's brain. My guess is that the lipids aren't due to injury, but might be an early signal in neurogenesis. Although the trauma can't be seen, it doesn't mean that it isn't there. I assume that the blasts break synaptic connections, and this probably initiates the production of new neural cells.
It seems, and obviously this is just one slide--likely their best one at that, that their marker is activated in the entire hippocampus, not just the specific neurogenic region. Hippocampus is required for memory formation. Perhaps this lipid is part of the underlying pathology that inhibits memory formation, probably on cog in a big wheel.
Neat extra commentary on your part, mk, but how would you test that hypothesis? Look for signs of small tissue damage? Add fluorescent markers for other pathways involved in neurogenesis? (Not a neuroscientist, so throwing words at walls to see what sticks)
One method that comes to mind is that you could apply the lipid itself and see if it stimulated neurogenesis. There are a number of protein markers for new neural cells, so detecting it is easy enough. I don't know too much about synaptic disruption, but staining for synaptophysin, which is a marker for synaptogenesis might reveal the repair of synapses after the injury.
Fore sure. I worked mostly in stroke, and yes, we would see it there. Interestingly, although neurogenesis was typically highest ipsilateral to the lesion, synaptogenesis was very robust in the contralateral hemisphere following injury. The thinking is that the uninjured hemisphere increases plasticity to compensate for what was lost in the other hemisphere. I don't know the details, but a colleague in our lab also observed new nerves crossing in the spinal column following stroke, possibly leading to same-side control in an effort to compensate for lost brain.Well, it could just be a by-product of the pathway.