In contrast to that, Hashimoto et al. found a protective effect of βSyn overexpressing neurons to the pesticide rotenone [28], while in the same year, 2004, Ohtake et al. reported two unrelated patients with LBD who had two different heterozygote mutations in the SNCB gene, postulating that the absence or dysfunction of βSyn may impair the normal inhibitory effect on the formation of toxic αSyn fibrils, thereby indirectly contributing to the pathogenesis of synuclein-related neurodegenerative diseases [29]. This evidence concerns the gene SNCG and neurodegenerative disease.