Prior to the development of pathology in AD model mice (3xTg-AD), impaired or inhibited proteasome activity can increase tau and Aβ accumulation, a process which can be rescued with Aβ immunotherapy against Aβ oligomers, reducing protein accumulation and restoring proteasome activity (Oddo et al., 2004; Oh et al., 2005; Tseng et al., 2008). The gene discussed is MAPT; the disease is Alzheimer disease.