In a mouse model of SCA6, BDNF and TrkB were downregulated at the age-at-onset, and early activation of TrkB-AKT signalling improved symptoms59, supporting our previously unappreciated findings whereby early manipulation of TrkB signalling regulated pathways in which GSH metabolism is crucial to halt the degenerative process triggered in iSPNs lacking BDNF-TrkB signalling. This evidence concerns the gene BDNF and spinocerebellar ataxia type 6.