The present study determined whether grafts of nerve growth factor-producing fibroblasts alter the expression of beta-amyloid in young or aged nonhuman primates. Aged monkeys serve as an animal model which normally exhibits beta-amyloid-laden plaques. Three young adult (7-12 years of age) and three aged (24-29 years of age) rhesus monkeys received intraventricular implants of polymer-encapsulated cells that were genetically modified to secrete human recombinant nerve growth factor (NGF). Three young adult and three aged rhesus monkeys received identical treatment except that the grafted cells were not genetically modified and thus differed only by a single gene construct. Five additional aged rhesus monkeys were ungrafted and also served as controls. Three to four weeks posttransplantation, young monkeys did not display beta-amyloid-immunoreactive profiles within any CNS structure regardless of treatment. Qualitative observations revealed that aged monkeys displayed numerous beta-amyloid plaque-like structures within the amygdala and hippocampus as well as limbic and neocortices. The amount of beta-amyloid immunoreactivity (beta-amyloid load) was quantified bilaterally within the temporal neocortex of these animals. The beta-amyloid load within the temporal neocortex of aged monkeys was highly variable but did not differ across treatment groups. These data indicate that chronic short-term administration of NGF does not affect the expression of beta-amyloid in the young or the aged primate brain.