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Moreover, drugs may improve cognitive function without altering A levels, which is in agreement with reports suggesting that the clinical phenotype is not always closely related with the A plaque numbers or load in postmortem AD brains (Aizenstein et al., A frameshift mutation in the ubB (ubiquitin) gene (UBB+1) selectively expressed in brain was associated with increases in neurofibrillary tangles and plaques in AD, Picks disease and Downs syndrome patients, but was not found in the healthy young population, which suggests a link between the UPS and AD pathogenesis (van Leeuwen et al., 1998, 2006)