SLC9A6 and neuroaxonal dystrophy: Additionally, the mice exhibit progressive Purkinje cell loss in the cerebellum, neuroaxonal dystrophy, and behavioural abnormalities, including hyperactivity and cerebellar signs.22 Recently, NHE6-deficient rats have shown age-related tau deposition with widespread distribution, such as cortical and subcortical regions, recapitulating tau pathology dependent on SLC9A6 loss of function.23 These findings underscore the importance of SLC9A6 in endosomal membrane trafficking, lipid homeostasis, and protein quality control, particularly in neurons.