In Parkinson's disease, the protein 'alpha-synuclein' aggregates within neurons of patients and appears to propagate across interconnected areas of the brain. How this happens remains largely unknown. It has been proposed that alpha-synuclein may behave like a 'prion.' However, recent findings reveal that pathology caused by alpha-synuclein does not necessarily involve prion-like seeding. Instead, it could be triggered by enhanced alpha-synuclein expression and trans-neuronal passage of monomeric and oligomeric forms of the protein.