Well, I'm going with the science, rather than some personal theories that very common SNPs which have little impact are conspiring to make 100% of the population very ill. Because that is basically where your theories seem to lead, mathematically speaking.
So Val, are you saying that there is absolutely no relationship between Parkinson's and Monoamine Oxidase SNPs?
The abstract is merely stating the frequency of genotypes. With no comparison to non-Parkinson's controls, it lacks any context and is quite meaningless. There also isn't any full text article available for that. No conclusions can be drawn regarding the affect of alleles.
Here is the
full abstact:
http://europepmc.org/abstract/med/25636089
"OBJECTIVE
To study polymorphisms of catechol-O-methyltransferase (COMT) and monoamine oxidase B (MAO-B) genes among Chinese patients with Parkinson's disease. METHODS
Genotypes of the COMT and MAO-B genes of 1408 patients with Parkinson's disease was sequenced using Sanger method. And these patients were recruited by Chinese Parkinson Study Group from 29 research centers throughout the country. RESULTS The genotypic frequencies of
COMT rs4680 AA, AG, GG were 8.9%, 42.0% and 49.1%. Those of rs4818 CC, CG, GG were 42.5%, 45.6% and 11.9%, respectively. The genotype frequencies of
MAO-B rs1799836 A/AA, AG, G/GG were 74.4%, 14.1% and 11.5%, respectively. The haplotype formed by
COMT rs4680 (GG) and
MAO-B rs1799836 (A/AA) genotype has a frequency of 36.86%. CONCLUSION Polymorphisms of
COMT and
MAO-B genes has a unique characteristics among Chinese patients with
Parkinson's disease. They may be related with differences in drug response in such patients."
If any other of you carefully look at the SNPs they are talking about you will find that all these high frequency SNPs in people with Parkinsons are the result of faster catecholamine depletion.
As to anxiety and MAO and COMT SNPS:
(Val, don't worry, I already know you will have a non paper backed up rebuttal on how these genes don't matter.)
http://hmg.oxfordjournals.org/content/8/4/621.short
One class of drugs effective in the treatment of panic disorder is represented by monoamine oxidase A inhibitors. Therefore, the monoamine oxidase A gene on chromosome X is a prime candidate gene. In the present study we investigated a novel repeat polymorphism in the promoter of the monoamine oxidase A gene for association with panic disorder in two independent samples (German sample,
n = 80; Italian sample,
n = 129). Two alleles (3 and 4 repeats) were most common and constituted >97% of the observed alleles. Functional characterization in a luciferase assay demonstrated that the longer alleles (3a, 4 and 5) were more active than allele 3. Among females of both the German and the Italian samples of panic disorder patients (combined,
n = 209) the longer alleles (3a, 4 and 5) were significantly more frequent than among females of the corresponding control samples (combined,
n = 190, χ2 = 10.27, df = 1,
P = 0.001).
Together with the observation that inhibition of monoamine oxidase A is clinically effective in the treatment of panic disorder these findings suggest that increased monoamine oxidase A activity is a risk factor for panic disorder in female patients.
http://www.jbc.org/content/279/38/39645.short
A spontaneous monoamine oxidase A (MAO A) mutation (A863T) in exon 8 introduced a premature stop codon, which produced MAO A/B double knock-out (KO) mice in a MAO B KO mouse colony. This mutation caused a nonsense-mediated mRNA decay and resulted in the absence of MAO A transcript, protein, and catalytic activity and abrogates a DraI restriction site.
The MAO A/B KO mice showed reduced body weight compared with wild type mice. Brain levels of serotonin, norepinephrine, dopamine, and phenylethylamine increased, and serotonin metabolite 5-hydroxyindoleacetic acid levels decreased, to a much greater degree than in either MAO A or B single KO mice. Observed chase/escape and anxiety-like behavior in the MAO A/B KO mice, different from MAO A or B single KO mice, suggest that varying monoamine levels result in both a unique biochemical and behavioral phenotype. These mice will be useful models for studying the molecular basis of disorders associated with abnormal monoamine neurotransmitters.
http://www.nature.com/tp/journal/v5/n1/abs/tp2014135a.html
Elevated hippocampal and cortical tyrosine hydroxylase, downregulated cortical monoamine oxidase-A levels, as well as increased hippocampal brain-derived neurotrophic factor (BDNF) and pro-BDNF support the flavanol’s anxiolytic effects. In addition, elevated pAkt in hippocampus and cortex was observed. (−)Epicatechin ingestion did not facilitate touchscreen performance or DG neurogenesis, suggesting a non-neurogenic mechanism.
The concurrent modulation of complementary neurotrophic and monoaminergic signaling pathways may contribute to beneficial mood-modulating effects of this flavanol.
http://link.springer.com/article/10.1007/s10517-015-2826-8#page-1
The development of behavioral disorders presented by low exploratory activity and
high anxiety was associated with transformation of catalytic characteristics of cerebral monoamine oxidases, associated with the development of oxidative stress with predominant intensification of metal-catalyzed protein oxidation.
http://www.sciencedirect.com/science/article/pii/S0191886915001749
We examined associations of COMT rs4680 and personality in older adults.
The COMT rs4680 GG genotype associated with lower Neuroticism scores.
GG genotype also associated with higher Agreeableness and Conscientiousness score
GG’s dopamine release might be optimal for a more adaptive personality profile.
Here is a whole book on the subject:
http://books.google.com/books?hl=en&lr=&id=pabKBwAAQBAJ&oi=fnd&pg=PA47&dq=COMT anxiety&ots=MjkADgccVz&sig=XCaPXH0FjzSn3AY8eWDVS32cIIY#v=onepage&q=COMT anxiety&f=false