Cognitive decline and synaptic plasticity deficits are reported to occur prior to the accumulation of Aβ plaques and tau neurofibrillary tangles in the prodromic phase leading to AD (Oddo et al., 2003), supporting the idea that synaptic dysfunction and mild cognitive impairment are early events driven by soluble oligomeric Aβ rising to abnormally high levels years prior to AD diagnosis. This evidence concerns the gene MAPT and Alzheimer disease.