Restoration of endogenous frataxin levels reverses neurologic and cardiac phenotypes associated with Friedreich's ataxia in adult mice even after significant motor dysfunction.

In Drosophila, the loss of Frataxin causes iron accumulation in the nervous system, which in turn enhances sphingolipid synthesis and activation of PDK1 and Mef2, which leads to neurodegeneration.

The iron/sphingolipid/PDK1/Mef2 pathway is activated in mammals upon loss of Frataxin.

Somatic instability of the CAG repeat increases progressively with age and disease progression in Huntington disease mutation carriers, starting with low levels in fetal brain tissues.

Signaling at the primary cilium is important to sustain the morphology, connectivity, and survival of a key neural population within the brain.

Expanded repeat RNAs associated with human neurodegenerative diseases can become incorporated into transported granules in neurons, perturbing their function to cause neuritic branching defects.

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