Accordingly, in agreement with the relevant developmental role of Contactins, changes in their expression profiles were suggested to sustain the pathogenesis of specific neurological disorders [90,91,92,93] and in the present study, we provide evidence about the potential involvement of Contactin 1 into the pathogenesis of the Friedreich Ataxia in which we report reduced Contactin 1 expression in both the cerebellar cortex and the spinal cord. Here, CNTN1 is linked to Friedreich ataxia.