Adolescent prodromal phenotypes of psychiatric disorders: insights from a novel DISC1-perturbed monkey model
Neurodevelopmental deficits frequently lead to mild but significant adolescent social and cognitive changes, representing prodromal manifestations of adult-onset psychiatric disorders in a cross-disease manner. Although experimental medicine utilizes animal models to address the mechanisms, rodent brains lack critical structures for human higher brain functions such as the dorsolateral prefrontal…
Adolescent manifestations of psychiatric disorders, characterized by subtle yet significant social and cognitive changes, share a common pattern across various diseases. Conventional animal models, primarily relying on rodents, fail to capture essential human brain structures, like the dorsolateral prefrontal cortex, which are crucial for higher brain functions.
To bridge this gap, scientists developed monkeys with an impaired DISC1 gene, a protein vital for neurodevelopment and implicated in transdiagnostic mental health risks. By minimizing mosaicism, researchers focused on F0 monkeys during their human-equivalent adolescent stage. These monkeys displayed diminished social responsiveness and heightened internal drives, aligning with altered social behaviors observed in humans during the prodromal stage of psychiatric disorders.
Resting-state functional MRI data from these monkeys revealed disrupted global functional connectivity and reorganized network topology, characterized by a shift in brain hub dominance from prefrontal regions to sensory areas. This primate model offers a distinctive platform for investigating psychiatric disorders, such as schizophrenia, throughout the developmental process.
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