Microarray analysis of nonhuman primates: validation of experimental models in neurological disorders

<jats:title>ABSTRACT</jats:title> <jats:p> Nonhuman primates (NHPs) have provided robust experimental animal models for many human‐related diseases due to their similar physiologies. Nonetheless, profound differences remain in the acquisition, progression, and outcome of important diseases such as AIDS and Alzheimer's, for which the underlying basis remains obscure. We explored the utility of human high‐density oligonucleotide arrays to survey the transcription profile of NHP genomes. Total RNA from prefrontal cortices of human ( <jats:italic>Homo sapiens</jats:italic> ), common chimpanzee ( <jats:italic>Pan troglodytes</jats:italic> ), cynomolgous macaque ( <jats:italic>Macaca fascicularis</jats:italic> ), and common marmoset ( <jats:italic>Callithrix jacchus</jats:italic> ) was labeled and hybridized to Affymetrix U95A GeneChip probe arrays. Corresponding data obtained previously from common chimpanzee and orangutan ( <jats:italic>Pongo pygmaeus</jats:italic> ) were added for comparison. Qualitative (present or not detected) and quantitative (expression level) analysis indicated that many genes known to be involved in human neurological disorders were present and regulated in NHPs. A gene involved in dopamine metabolism (catechol‐O‐methyltransferase) was absent in macaque and marmoset. Glutamate receptor 2 was up‐regulated, and transcription‐associated genes were down‐regulated in NHPs compared with humans. We demonstrate that transcript profiling of NHPs could provide comparative genomic data to validate and better focus experimental animal models of human neurological disorders. </jats:p>