I came here to post about the same paper
@SNT Gatchaman 
Thanks guys, I searched a bit for cross-binding problems but didn't find anything as specific as that.
It would make good sense. The pictures look most like images of CGRP neurons but I haven't seen any images specifically of ACh neurons so they may be the same.
So the first conclusion is that this may not be amyloid at all. Since the findings didn't seem to tie in with Pretorius anyway that may not take us much further.
But if this is staining of cholinesterase there are two possibilities. One is that this is a sampling artefact. Maybe muscle wasting (of which there will be at least some in ME and LC) may mean that nerve endings make up a higher proportion of tissue per cross sectional area and so on.
The other possibility would be much more interesting - that there is actually more cholinesterase around in nerves going to muscle (and arteriole - in muscle at least).
Now that would lead to a really fancy theory!
I like to play S4ME exactly the way we played debating B cells in my lab 25 years ago - throwing out any idea that arrives and then shredding it - until one day an idea wouldn't shred. Trendy ideas get short shrift but sometimes they turn out a bit right.
There is maybe a possibility that the inability to generate action in ME and LC links to a regulatory mechanism that normally after infection kicks in to calm down any too violent return to hunting mammoths. The mechanism might pivot upon regulating cholinesterase. The effect would be a bit like the soft pedal on a piano. You can still make a lot of noise if you really bang the keyboard but it becomes increasingly effortful and soon enough you give up trying. There may also be regulatory mechanism centrally that pick up the effect of the peripheral regulation and turn off neural control even higher to prevent getting into situations where exertion is costly.
This would make ME or LC remarkably analogous to myasthenia graves, where the ACh receptors are blocked. But rather than producing weakness it might tend to produce a failure in follow through that manifest as a rather different form of fatiguability.
The next question would be what made the nerve or muscle cells express more cholinesterase. That would be easy. It could easily be regulated by policing T cells or macrophages primed by T cells. It could also be regulated by painting signalling molecules on to supportive microfibrils such as fibrillin-1. Such processes would take hours or days so would explain delay in PEM.
Now for the shredding.
