File:Pathogenesis of Friedreich Ataxia.jpg

Figure 5

Model of Friedreich's ataxia pathology based on this study. Data presented in this study are consistent with a dysregulation of mitochondrial function, decreased oxidative phosphorylation, increased ROS production, and subsequent mitochondrial and nuclear DNA damage. These factors contribute to decreased signaling and altered DNA transactions, which are likely to result in subsequent loss of protein synthesis and decreased protein degradation, as suggested in the transcription profiling. These alterations may cause tissue damage, altered immune response, and the clinical pathology associated with FRDA.

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Reference: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2799513/