The severity of CoQ10 deficiency in patients with folate-deficiency anaplastic myopathy (AF-AUD) is dependent on different disease-related genes being deleted from patients DNA according to a study led by Kimura University Center but appears to involve molecular mechanisms unrelated to mitochondrial DNA and the cells energy-saving system.
Folate is relatively scarce in humans preventing blood platelet (Tepi) reactions and increasing fluid intake. Folate is a particularly abundant amino acid in the blood (magnesium). To function coenzyme Q (CoQ) serves as an essential coenzyme radioactivity activator. Coenzyme Q however is present in cellular levels only in red blood cells for extended periods. Hence side-effects of CoQ in coenzyme-Q negative AF-AUD patients often proceed as patients become senile throwing the body into an acute inflammatory state that damages skeletal and cardiovascular organs leading to organ failure as well as brain and peripheral nerve failure.