The accumulation of extracellular senile plaques and intracellular aggregates, composed of β-Amyloid, and the intracellular accumulation of neurofibrillary tangles comprising hyperphosphorylated variants of the protein tau and UBB+1, the frameshift variant of ubiquitin B, contribute to AD progression (van Leeuwen et al., 1998; Laferla et al., 2007; Benilova et al., 2012; Mandelkow and Mandelkow, 2012). Here, UBB is linked to Alzheimer disease.