For example, the GBA1 (glucocerebrosidase1) deficiency induces GSL (glycosphingolipid) accumulation, whichcould destabilize the helical αS tetramer and other multimersin the dopaminergic neurons and promote self-assembly of monomersto toxic αS oligomers.20 Moreover,very recent in vivo preclinical data indicate thatWT GBA1 in PD-like mice improves the tetramer to monomer ratio andαS solubility. The gene discussed is CTSA; the disease is Parkinson disease.