@article {Watanabe2020.08.18.255240, author = {Satoshi Watanabe and Tohru Kurotani and Tomofumi Oga and Jun Noguchi and Risa Isoda and Akiko Nakagami and Kazuhisa Sakai and Keiko Nakagaki and Kayo Sumida and Kohei Hoshino and Koichi Saito and Izuru Miyawaki and Masayuki Sekiguchi and Keiji Wada and Takafumi Minamimoto and Noritaka Ichinohe}, title = {Distinct synaptic and related transcriptional abnormalities in neonatal, childhood and mature autism model of primate: implications for early-age therapeutic intervention}, elocation-id = {2020.08.18.255240}, year = {2020}, doi = {10.1101/2020.08.18.255240}, publisher = {Cold Spring Harbor Laboratory}, abstract = {Autism spectrum disorder (ASD) is a synapse-related disorder that is diagnosed at around 3 years of age. Earlier intervention is desirable for better ASD prognosis; however, there is limited biological literature regarding early-age ASD. This study aimed to assess altered cortical synapses and gene expression in the ASD model marmoset. There were distinct phenotypes in the model animals across the neonate, childhood, and mature stages in the dorsomedial prefrontal cortex (Brodmann area 8b/9). At the neonate stage, synapses were underdeveloped and modulated genes were enriched with synaptogenesis- and ASD-related genes. At the childhood stage, synaptic features and gene expressions associated with experience-dependent circuit remodeling were altered in model animals. At the mature stage, there were synapse overdevelopment and altered gene expression similar to those in human ASD. These early synaptic phenotypes and altered gene expressions could be novel targets of efficient therapy from a young age.Competing Interest StatementThe authors have declared no competing interest.}, URL = {https://www.biorxiv.org/content/early/2020/08/18/2020.08.18.255240}, eprint = {https://www.biorxiv.org/content/early/2020/08/18/2020.08.18.255240.full.pdf}, journal = {bioRxiv} }