MAPT and Alzheimer disease: Consistent with these findings, pharmacological inhibition of the proteasome leads to increased levels of β-amyloid peptides (Aβ) and tau (Tseng et al., 2008), which contribute with the extracellular deposits known as amyloid plaques consisting of Aβ (Masters et al., 1985) and the formation of intracellular neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau (Braak et al., 1986), two AD pathological hallmarks.