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(The Company of Biologists) Current treatments may be administered too late to target Friedreich's ataxia effectively. New research using a slow-onset frataxin knock-in/knockout mouse model showed significantly reduced levels of mitochondrial biosynthesis proteins and early mitochondrial deficiency in the cerebellar cortex, even at pre-symptomatic stages of development. This suggests that the progressive degeneration in mitochondrial function seen in individuals with Friedreich's ataxia is not only the mechanism causing the disease, but also a potential biomarker and therapeutic target.
Original Article: Early intervention may hold key to treatment of Friedreich's ataxiaNEXT ARTICLE