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Impairment associated with glutamatergic/calcium signaling has become pointed in a variety of sporadic and anatomical ataxias, such as SCA6, SCA13, or SCA27. SCA6 is a member of the CAG enlargement inside the CACNA1A subunit with the voltage-gated calcium supplements channel P/Q CaV2.1. Boost in calcium mineral signaling leads to the gain-of-function, and also translocation of the fragment on the

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