Moreover, on the basis of amyloidtheory and genetics of AD, arising dependency on transgenic AD models possessing the targets ofamyloid plaque and tau protein has been witnessed.13 Additionally, the mouse brain produces amyloid peptidesdistinct from the human brain, and the mouse model, even with amyloiddeposition, often fails to show a substantial neuronal loss.14 Moreover, comorbidities associated with humanAD are not well-mimicked in animal models. This evidence concerns the gene MAPT and Alzheimer disease.