In order to make progress in deciphering biological mechanisms at play in DLB including GBAe32 and inflammatory pathways,e33 it will be necessary to develop robust animal models that capture the true neuropathologic and behavioral abnormalities of DLB, and to identify possible disease-specific molecular differences in α-synuclein, tau, and Aβ among DLB, PD, PD dementia, and AD. This evidence concerns the gene SNCA and Alzheimer disease.