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Genotype frequencies Melastatin M3 and muscarinic receptor gene polymorphism

Kati

Patient in training
Messages
5,497
Genotype Frequencies of Transient Receptor Potential Melastatin M3 Ion Channels and Acetylcholine Muscarinic M3 Receptor Gene Polymorphisms in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis Patients

Full paper access: http://www.la-press.com/genotype-fr...m3-ion-article-a5387-abstract?article_id=5387

By Dr Marshall-Gradisnik and team

100 patients with ME/CFS and 90 healthy controls.



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allyann

Senior Member
Messages
418
Location
Melbourne Australia
Muscarinic AChRs (mAChRs) are involved in autonomic function, particularly parasympathetic and exocrine function, such as in pancreas, exocrine glands, and inotropic and chronotropic cardiac regulation. Given that AChRs are distributed differentially around the body, it is axiomatic that tissues expressing a predominance of these receptors will be affected differentially by SNPs in muscarinic vs. nicotinic AChRs. Similarly, TRPs are distributed differentially around the body in all tissues. Adding to the complexity is the relative lack of knowledge about interactions between TRP and AChRs in humans. Interestingly, certain muscarinic ACh receptors are antagonists of TRPM3 via, for example, phospholipase C-coupled muscarinic ACh M1 receptor (mAChM1R).21,22 Given this developing research regarding the interdependence of mAChRs and TRP families, we question whether specific mAChM3R and TRPM3 SNP genotypes in CFS/ME contribute to the pathomechanism and phenotypes of this illness.

From my understanding Muscarinic receptors are responsible for cognitive functions, so this research would explain the brain fog???
 
Messages
15,786
For all of those SNPs, the authors are claiming that the genotypes with the more common allele are the ones associated with risk. Which means most healthy people will have several "risky" genotypes, according to that table.

They are also calculating percentages in a really bizarre manner. Instead of showing the actual frequency of the genotype for each group, they're showing the percentage of that genotype for each group out of the total prevalence in both groups combined.

This might be a valid approach if each group (patients and controls) is the same size, but they are not. There are 100 patients and 90 controls, which gives a big boost to the patient group, so of course the patient percentages are higher.

As a result, the comparisons in that table are probably meaningless. And if the differences stood up with a normal frequency comparison, they probably wouldn't have made this type of comparison in the first place.
 
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Deltrus

Senior Member
Messages
271
Interesting, since muscarinic acetylcholine receptors are anti-inflammatory and extremely dense in the parasympathetic nervous system (including the vagus nerve), then perhaps overexpression of these receptors can allow for infection of the vagus nerve. In addition, these receptors are very stimulating to the parasympathetic nervous system, potentially forcing the body into "rest and digest mode".