Because the overexpression of humanized αsyn in mice expressing all six isoforms of tau produced only minor changes in neuropathology, motor, and cognitive behavior at both 6- and 9-MPI and poorly recapitulated deficits observed in DLB, we decided to evaluate whether AAV-induced humanized tau overexpression in an established transgenic model of αsyn overexpression would aggravate or accelerate the behavior and pathology. The gene discussed is MAPT; the disease is Lewy body dementia.