Hi Freddd,
Warning long post incoming
My thoughts: (wish they could be more upbeat and happier)
Alzheimer's is unbelievably complicated and almost all of the old theories have been washed out (tau phosphorylation, beta secretase, etc.). No one knows. But ... too much of the population gets ALZ at some point (if they live long enough) for it to be one or two genes involved. I think the prevailing view is multiple points of failure + epigenetic stresses. Again it is highly controversial. So I would not go there attempting to explain by any theory. Quite frankly it will fail given the complexity. It is so bad that the current mindset is to focus on diagnosis and not treatment right now. I know these are things people don't want to here but it is what is going on right now. Our civilization is still behind the eight ball on that disorder. So while correlative risks may be teased out on early diagnostics, mechanism is highly uncertain. The fact that ALZ has low CSF b12 or issues with MMA or HCY, I fear doesn't really mean much. The CNS for an advanced ALZ patient is completely borked. Many measurements will be jacked. Do you know how much working brain matter a person with full blown ALZ has when the diagnosis was made in say the 1980s-1990s? 20-25%. Meaning if you cut open their skull and peaked inside, only 20-25% of cells were functional. Low biomarkers for the variables you mentioned I don't think mean much when 75% of brain matter has been turned into a wasteland.
MS is a different story. The latest epidemiology studies and latest research really seems to point to a CNS autoimmune attack instigated by infection by a normally benign virus that prefers cold weather climates yet in some cases crosses the blood brain barrier. The result of being in the "wrong place" leads to microglia activation generating antibodies that attack white matter as per an autoimmune attack. You mention these other biomarkers, but inflammation is very central to MS. We just still do not know the antibody unfortunately. Some experts still disagree on this, but this virus to BBB crossing to CNS autoimmune link is becoming more and more crystallized. It is being forced onto the medical community based on careful diagnosis, patient history, and epidemiology analysis. There are a couple of genes that are considered risks for MS but I don't believe they have commonality to any of the other diseases you mentioned.
Parkinson's is more murky. There are a couple of competing theories, though at least one of the classical ones is fading. Again an inflammatory condition that wrecks havoc in the substantia nigra part of the brain. This theory has come on strong of late since large scale studies of anti-inflammatories have showed a 15% or more (more for longer use) reduction in incidence of Parkinson's ... which is huge. Sorry I don't know more than that.
Autism of course a broad spectrum disorder and while methylation seems to be an interesting means to help improve symptoms, the underlying cause and mechanism suggest defects in MANY genes + epigenetic factors during development in the womb. As an example of a totally different sort (and not autism, so people do not get all upset), Down's syndrome involves a massive deletion of a chromosome. My point is genetic defects do not have to be only point mutations. If only that were true it would make the world of bioinformatics a much simpler place.
So to be perfectly honest on your question. I have no idea. I would bet my mortgage that it is not one or even a small number of genes. I would also further bet that most of the disorders you mentioned the genotype correlation is very low. I don't think we are looking for haplotypes with low linkage disequilbrium. Certainly not for ALZ. Not a chance. I think some of the disorders involve gene regulatory 'concert' defects while others involve breakdowns due to epigenetic factors (like a viral infection that gets into the CNS).
My suspicion (and I know this may not be popular but what the hey) is there are multiple neurological disorders with many different causes that can end up producing low biomarkers related to methylation and folate cycles in the CSF. A similar analogy is there are many disorders that ultimately lead to hormonal dysregulation and adrenal fatigue. But the causes can be very different for each disorder that brought us to a similar place. Then again defects in genes that regulate the methylation and folate cycles won't help matters if "stress" is being put on those systems by virtue of epigenetic triggers that launch neurological disorders.
I can't remember where it is now, but someone did a meta-analysis of fibromyalgia and determined a significant number of those diagnosed had hormonal problems. So which is the chicken and which is the egg? Some patients have high RT3 values, take Cytomel and they are in remission. Others that treatment does zilch. The reason I bring this up is I sadly feel CFS and Fibro are classifications that help doctors but with many diverse causes that lead to similar metastable (but bad) health states with certain similar symptoms. I think methylation and folate and ATP treatments have value because they try to get the body to heal itself and develop some sort of homeostasis. But I don't think that means their genes in those cycles doom them to CFS/ME.
Heck personally I see a lot of people on here with bad health states but with honestly not that bad of genotypes (at least for SNPs we know of). Also though I am on these boards ... I don't have CFS. Rich and I arrived at that conclusion a couple years ago looking at a NutraEval from Genova and multiple other labs. Later I learned I have an autoimmune disease of the CNS (and periphery) and not a benign one. So why am I here? Because supplementing for the folate and methylation cycles helps me with some (I note SOME) of my symptoms. On the other hand if you took my glucocorticoids away from me, you might as well put a gun to my head. My point, as unsatisfying as it may be, is there may be MANY causes or triggers, but so many of us end up in similar places and treating some of the most fundamental biochemical cycles is one of only ways after years and years of damage to get the body to do some constructive rebuilding from the inside.
Sorry if that was not the answer you were looking for. But it is what I think. I wish I could give a simpler and more empowering insight. I am almost positive that a simple straightforward genotype association does not exist across the spectrum of disorders you mentioned. Of course they have relevance but the outcomes are very nonlinear.
For example in three generations my paternal family line has one case of SPS (me), one case of MS (aunt), and two cases of ALS (grandfather and his first cousin). I mention that to a neurologist and their eyes nearly bulge out of their head, then they relax, start to think, smile and I start to worry they are sizing me up for vivisection to get DNA samples (just kidding). On the other hand the same paternal family line but through my paternal grandmother had two cases of terminal ovarian cancer. Guess what all the other aunts did when all that went down? So in one case the genetics is probably important but unbelievably cloudy and complicated since we had three vastly different diseases for four people, in the other case the genetics is more straightforward since my grandmother and her daughter both had the same condition (though they responded to treatment very differently, one was known ahead of time and fought for a long time, the other was a shock and died almost instantly).
What I do think is that low biomarkers for methylation and folate cycles, means those cycles are in jeopardy in the CNS and the best we can do is try to fortify them. And hey for many of us that is very helpful. You and I each in our ways have beat (or I should say are defying) odds that were stacked against us. Doesn't mean a cure but can mean a really significant improvement that holds back the red tide.
Take care.