By measuring targeted CSF d18:1 isoforms of various sphingolipid species (d18:1 GlcSph, GalSph, d18:1, 18:0 Cer, GlcCer, and SphM) in a multi-center cohort comprising 152 PD and 37 DLB participants with and without various heterozygous GBA1 variants and 40 HC we found no clear increase of the key substrates GlcCer and GlcSph when comparing GBA1 variant carriers with their WT comparator group. The gene discussed is GBA1; the disease is Parkinson disease.