However, the most accepted hypothesis of AD is amyloid cascade hypothesis[112], which posits that amyloid-β (Aβ) accumulation is the primary event leading to a cascade of effects that result in neuronal damage while hyperphosphorylated protein (e.g., p-Tau) tangles, the second hallmark of AD, is a downstream effect of Aβ accumulation. This evidence concerns the gene MAPT and Alzheimer disease.