The key finding from our study is that the PD- and MSA-PMCA αSyn fibrils, with their similar protofilament fold but distinct quaternary arrangement, have different activity when added to mouse primary oligodendroglial cultures: the MSA-PMCA fibrils are more potent in recruiting the endogenous oligodendroglial αSyn and evoking a redistribution of TPPP/p25α protein when compared to the PD-PMCA fibrils (Fig. 1). The gene discussed is TPPP; the disease is Parkinson disease.