title: Preservation of prefrontal cortical volume in behaviorally characterized aged macaque monkeys.
abstract: Normal aging is frequently accompanied by a decline in cognitive capacities supported by the prefrontal cortex. The principal aim of the present study was to determine whether these impairments are coupled to morphometric alterations affecting the volume of the prefrontal cortex in an established nonhuman primate model. A large sample of 19 young (4-11 years old) and 40 aged (20-32 years old) rhesus monkeys was tested using a delayed response procedure known to require the functional integrity of area 46 of the prefrontal cortex. Aged monkeys displayed robust delayed response deficits that were specifically related to the demands of testing on memory. Modern stereological methods were then used to estimate the total volume of area 46 and the volume of layer I in brains from 21 young and aged monkeys. Prefrontal cortex volume was entirely preserved in the aged monkeys as a group and among the subset of aged subjects that displayed the most severe behavioral impairment. These findings indicate that gross morphometric alterations affecting cortical volume are unlikely to account for age-related decline in the information processing capacities of area 46 in primates. Taken together, current evidence instead suggests that changes in the functional connectivity of critical cortical circuits may contribute to normal cognitive aging.
authors.affiliation: Kastor Neurobiology of Aging Laboratories, Mount Sinai School of Medicine, New York, New York 10029, USA.
authors.forename: K A
authors.initials: KA
authors.lastname: O'Donnell
authors.forename: P R
authors.initials: PR
authors.lastname: Rapp
authors.forename: P R
authors.initials: PR
authors.lastname: Hof
mesh_terms: D000375:Aging / Q000473:pathology* / Q000523:psychology; D000818:Animals; D001522:Behavior, Animal; D005260:Female; D008253:Macaca mulatta / Q000033:anatomy & histology / Q000254:growth & development*; D008297:Male; D008569:Memory Disorders / Q000209:etiology / Q000473:pathology; D017397:Prefrontal Cortex / Q000473:pathology*; D012153:Retention, Psychology / Q000502:physiology