We have also previously reported α-synuclein with putative pathological properties in the brain tissue of children with Krabbe disease and metachromatic leukodystrophy, sphingolipid storage disorders caused by Lewy body disease risk genes, suggesting a direct link between deficient sphingolipid homeostasis and α-synuclein aggregation [16, 17]. The gene discussed is SNCA; the disease is Lewy body dementia.