A slower clinical decline at follow-up was associated with deposition of LBs in the olfactory bulb and brainstem, while the early deposition of LBs in the limbic regions was associated with AD-like characteristics (APOE ε4 carriers, AD pathology and cognitive functioning)[10], which highlight that the diverse involvement of brain regions, along with associated AD risk factors, might results in heterogeneous DLB presentation. Here, APOE is linked to Alzheimer disease.