APP/PS1/Aβ-Th1 mice showed significantly increased dense amyloid plaque loads in cortex (p < 0.05, 86%) and hippocampus (p < 0.01, 134%) compared to APP/PS1 controls, while APP/PS1/Aβ-Th17 mice showed dense amyloid plaque loads 47% and 64% higher than APP/PS1 controls in cortex and hippocampus, respectively, but without significance. The gene discussed is APP; the disease is amyloidosis.