Difference between revisions of "User talk:Z3332250"
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Iron potential as treatment for FA is greatly focused. pathogenesis of FA is due he mitochondrial accumulation of Iron, causing a usage of cytosolic iron<ref name="PMID:10805340"><pubmed>10805340</pubmed></ref>.
Revision as of 23:18, 10 September 2011
Iron chelations potential as treatment for FA is greatly focused. Regarding pathogenesis of FA is due to he mitochondrial accumulation of Iron, causing a usage of cytosolic iron.Where most potential chelators are those which specifically target mitochondrial pools of iron.There is evidence that due to the fractin deficiency results in FA caused from the depletion of cytosolic iron, it has been suggested therapeutic treatment of iron supplements to replenish cytosolic iron to normal.
Articles to read:
friedreich Ataxia (FA) a progressive neurological congenital disorder, wtih no treatment identified only possible pharmaceutics which can reduce the progression of FA however not significantly. Whereas significant treatment poties of FA or reduction in progression are the following:
- Coenzyme Q10 and Vitamin E
Antioxidants treatment of FA which have shown most promise is Idebenone and Coenzyme Q10 with Vitamin E. Antioxidants have shown degree of reduction on oxidative stress in mitochondria though are still going through clinical trials.Conenzyme Q10 an electron carrier with a reduction of oxidative stress effect from the combination of vitamin E, combination of Q10 and vitamin E displayed a positive effect. Where Q10 and vitamin E conveyed the cardiac and skeletal improvement with the betterment of the mitochondrial synthesis.
Idebnone operates with a duel function where reversing redox reactions affecting electron balance in the mitochondria while also supporting mitochondria functions preventing damage.