Hence, intersubject differences in active neuronal circuity, density of synaptic terminals, plasma membrane molecules that bind/transport α-synuclein, pinocytic rates, membrane surface area, axon length, and the degree of myelin coverage could underlie variations in α-synuclein aggregate engulfment and partly explain the diverse clinical outcomes of Lewy body disease. The gene discussed is SNCA; the disease is Lewy body dementia.