"The influence of these genes is probably not large enough to be immediately used as a diagnostic tool. But the result "is an advancement of the understanding of migraine biology," he said."
And indeed that is what interests me. I haven't had a chance to really study these genes in detail, but if you read both the reports above, it appears some clarification may have emerged in another area as well.
We already know that idiopathic pain is a major problem in chronic disease, and we know that the individual's ability to properly sense the world around them is damaged. From the Wellcome story:
"By associating a variant that affects the gene LRP1 with common migraines, this confirms that the glutamate signalling pathway is involved in the development of migraines," says Professor Aarno Palotie, Senior Group Leader at the Wellcome Trust Sanger Institute and one of the authors of the study."
(Aha - so that is why Wellcome press release didn't give us the warning about the lack of immediately usefulness of the study results -- they sponsored the study and had an interest in it being successful)
Monosodium glutamate was always a big no-no for me... Isn't this getting interesting now...
AFP adds more info:
Two of them, known as PRDM16 and TRPM8, were specific to migraines, as opposed to other kinds of headaches. TRPM8, in addition, was linked to migraines only in women. Earlier studies have shown that the same gene contains the genetic "blueprint" for a pain sensor, in both men and women. The third suspect gene, LRP1, is involved in sensing the external world and in chemical pathways inside the brain.
So I guess future researchers can look at TRPM8 with respect to idiopathic pain. I wonder if there are any bacterial genes with close homology (similarity) to the 'mutated' TRPM8?
And the possibility that LRP1 might lead to part of the answer for syndromes such as MCS (multiple chemical sensitivity) does intrigue me, as my migraines were often associated with an increased sensitivity to objectionable stimuli - mostly smells.