In order to test the theory that an aggregation prone form of αsyn could induce endogenous physiologic αsyn to form pathologic inclusions, sections of hippocampus and midbrain were obtained from a Contursi kindred patient in which familial PD/LBD developed due to a heterozygous A53T mutation in the SNCA gene [27]. The gene discussed is SNCA; the disease is Parkinson disease.