Neuropathologically, DLB is defined by the accumulation of α-synuclein and the formation of Lewy bodies and Lewy neurites, although autopsy studies have revealed that up to 70% of individuals with DLB also exhibit co-existing extracellular amyloid-β plaques and intracellular paired helical filaments of tau, both of which negatively impact disease progression, prognosis, and survival2–4. This evidence concerns the gene MAPT and Lewy body dementia.