Sunday, August 12, 2012 2:24 PM
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Tony Miles
http://www.biomedcentral.com/content/pdf/1471-2350-13-70.pdf "Conclusions Polymorphisms in the genes coding for iron binding and transporting proteins, in the presence of local iron overload, might be responsible for suboptimal iron handling. This might account for the significant variability peculiar to MS phenotypes, particularly affecting MS risk and progression paving the way for personalized pharmacogenetic applications in the clinical practice." "Conclusions Whatever the mechanism causing brain iron deposition is, our study shows strong influence of gene variants in MS onset and disease course in terms of expectation of disability and severity. Although, in our survey the homozygous prevalence of the investigated SNPs is low, ranging from 3% to 8%, we have to take into account that more than 80% of our patients carry at least one of these variants, and that about 50% are double carrier. On the basis that, combined carriers can have phenotypic effects greater than or comparable to single homozygotes, and that iron homeostasis is multi-genetically tuned, this opens new clinical concrete perspectives in monitoring iron accumulation as an underlying mechanism connected to the natural history of MS together with the prognostic value of iron trafficking genes. People carrying at risk alleles could be selected in advance for therapeutic trials aimed to iron chelation and dietary modification in the view that MS course could be in part genetically targeted. So, further larger investigations on iron genes should become mandatory in MS. Understanding the exact mechanism by which iron acts in the brain causing MS and how the brain would be impacted by iron chelation/supplementation could potentially furnish precious prognostic information and novel insights for alternative personalized treatments (pharmacogenetic) aimed in preventing or counteracting neuron loss and degeneration. All this is in line with a recently published review, on the importance of individualised therapy in MS, based on genetic and biochemical determinations
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