Table 1.

Historical milestones in Friedreich’s ataxia.

1863–1877	Friedreich [6–10] publishes extensive descriptions of FRDA.
1907	Mott [11] provides an extensive neuropathological description of a single case of FRDA, including the lesion of the dentate nucleus.
1957	Urich et al. [12] emphasize the existence of “suprasegmental” lesion in FRDA.
1980	Lamarche et al. [13] discover minute iron-positive granules in the cardiomyocytes of patients with FRDA.
1996	Campuzano et al. [1] identify the mutation in FRDA, name the lacking protein frataxin in analogy with FRDA, and recognize its role in iron metabolism.
1997	Rötig et al. [14] discover “iron–sulfur” protein deficiency (complexes I, II and III of the mitochondrial electron transport chain), and aconitase in endocardial biopsies of FRDA patients.
2002	Mühlenhoff et al. [15] recognize the importance of the yeast homolog of frataxin in the biogenesis of iron–sulfur clusters (Fe–S); Fe–S cluster deficiency is accepted as a critical factor in the pathogenesis of FRDA.