Lohle et al. (2015) [19] examined 110 individuals with GLA mutations (60 heterozygous females and 50 affected males) and found that, while individuals with confirmed GLA mutations do present some elements of a bradykinetic motor phenotype, including slower gait and lower hand speed, these individuals did not report the classic prodromal features of PD (hyposmia/anosmia, autonomic dysfunction, REM Sleep Behavior Disorder), as previously found in individuals with GBA mutations [20]. This evidence concerns the gene GBA1 and Kallmann syndrome.