The paper you linked by Hautakangas et al. found 123 associated loci with GWAS. I'm presuming you're looking at mutations at some of these loci as your markers for drug susceptibility.
My question: how much of the variance of migraine incidence do these loci explain? And what % of migraine sufferers do you expect will have a genotype that'll allow for a more targeted therapy?
Your site references a big increase in treatment effectiveness for patients on ineffective therapy – do you know how this would compare to patients changing medicines in a standard setting (w/o DNA testing)?
Mometricsmoproblems3 karma
The paper you linked by Hautakangas et al. found 123 associated loci with GWAS. I'm presuming you're looking at mutations at some of these loci as your markers for drug susceptibility.
My question: how much of the variance of migraine incidence do these loci explain? And what % of migraine sufferers do you expect will have a genotype that'll allow for a more targeted therapy?
Your site references a big increase in treatment effectiveness for patients on ineffective therapy – do you know how this would compare to patients changing medicines in a standard setting (w/o DNA testing)?
Thanks!
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