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The migraine has been shown to be associated with low KCNK18 activity and high blood levels of homocysteine. The SSHD-KC18/MTR molecules target the KCNK18 and MTHFR genes.
What do the genes KCNK18 and MTHFR do?
The KCNK18 gene encodes a protein called TRESK, a TWIK-related spinal cord potassium channel that is involved in manifestation of pain.
Migraine and severe headaches are two of the most common debilitating disorders. After many years of investigation, it has now been recognised that reduced activity of TRESK plays a major role in increased susceptibility to the onset of migraine and severe headaches. This finding was the result of a large international investigation, see Ref. 1 and within, results of which was summarised in an article by the Migraine Trust .
These important studies have identified that reduced activity of the gene KCNK18, which encodes the pain controlling protein TRESK, which, as indicated above, plays a major role in development of migraine and severe headache. The SSHD-KC18/MTR molecules target the KCNK18 and MTHFR genes.
In recent years, another important contributory factor has been recognised that increases susceptibility to development of migraine, and that is, a high level of the toxic amino acid homocysteine in the blood, see within Ref. 3.
The MTHFR gene encodes an enzyme called methylenetetrahydrofolate reductase, an enzyme involved in homocysteine degradation. The MTHFR gene product plays an important role in the conversion of 5, 10-methylenetetrahydrofolate to 5-methyltetrahydrofolate. This conversion reaction is required for the multistep process that converts the amino acid homocysteine back to another amino acid, methionine.
Decreased activity of MTHFR leads to inefficient conversion of homocysteine to methionine leading to a build up of homocysteine in the blood. High levels of homocysteine in the blood is not only associated with increased susceptibility to development of migraine but many other serious disorders such as heart disease, stroke, hearing loss and blood vessel deterioration, [see Ref. 4].