Brain prolyl oligopeptidase activity is associated with neuronal damage rather than beta-amyloid accumulation.

Prolyl oligopeptidase (POP) have been suggested to participate in the pathogenesis of Alzheimer's disease (AD). In this study the activity of POP is evaluated in AD patients and in transgenic mice with substantial deposits of beta-amyloid (Abeta). In AD cases, the POP activity displayed a significant negative correlation with the scores of senile/neuritic plaques and neurofibrillary tangles but not with Abeta-load. The transgenic mice with high levels of Abeta did not have altered POP activity compared to wild type mice. Based on our results, the low POP activity in AD seems to be associated with neuronal degeneration rather than to Abeta accumulation.