Globally, severe GBA mutations cause a more aggressive clinical phenotype, characterized by an earlier age at onset, more rapid axial motor progression, and more serious non-motor symptoms (hyposmia, sleep disturbances, dysautonomia, hallucinations, cognitive decline, and dementia) [177,181,190], consistent with the pathological, biochemical, and imaging biomarkers, showing more prominent nigrostriatal degeneration, reduction in neocortical metabolism [190], and lower levels of cerebrospinal fluid α-Syn [191]. Here, GBA1 is linked to Mental deterioration.