Not incompatible theories. The effects of the enzyme most likely vary with the type of cells. Neurons with really long axons would have more myelin to be affected. So, even if there was a brain-wide alteration in this enzyme or its metabolites, it might have significant effects on a few neurons while others are insignificantly affected.Thought it was a few cells in the brain.
ME doesn't seem to affect all brain cells equally. One can have serious brainfog, but not have impaired vision due to visual cortex neurons failing to the same degree. Some people suffer hypersensitivities in one sense, while others have it in a different sense, and others have none.
The theory of ME involving a small number of specific cells is more an explanation for why there's no obvious marker (all brain cells showing signs of mitochondrial dysfunction, or whatever).
I'm wondering whether a much larger percentage of the population has the ME root mechanism, but it'--by random chance--not affecting the part of the brain that leads to the common constellation of ME symptoms. Some people could be suffering from some ME symptoms, via the ME mechanism, but don't fit the ME criteria, so they're stuck with symptoms from a mysterious cause. Maybe chronic fatigue is ME with part of the mechanism not active.