Oligomeric forms of Aβ were found to be abundant in synapses of AD patients early in the disease before the appearance of phospo-tau at later stages, suggesting that soluble Aβ oligomers in synaptic terminals are associated with dementia onset and may initiate a cascade that drives phosphorylated tau accumulation and its synaptic spread [16]. This evidence concerns the gene MAPT and Alzheimer disease.