This synergy is also seen in mouse models of PDD/DLB: transgenic mice overexpressing both human β-amyloid and α-synuclein have higher levels of LB pathology and greater memory deficits than mice expressing just α-synuclein38; and double transgenic mice overexpressing two AD-related genes (amyloid precursor protein and presenilin 1) have greater amounts of α-synuclein as well as β-amyloid than mice transgenic for one mutation alone39. This evidence concerns the gene SNCA and Alzheimer disease.