A new study published by Cell Press in the February 25 issue of the journal
Neuron, manipulates a known schizophrenia susceptibility gene in the brains of fetal mice to begin to unravel the complex link between prenatal brain development and maturation of information processing and cognition in adult animals.
Schizophrenia is an incredibly complex and profoundly debilitating disorder that typically manifests in early adulthood but is thought to arise, at least in part, from pathological disturbances occurring during very early brain development.
"Although it is clear that multiple factors are involved in schizophrenia, many studies have suggested that variations in disease susceptibility genes might contribute to disruption of high brain functions such as cognition and information processing," explains study author Dr. Akira Sawa from the Department of Psychiatry at the Johns Hopkins School of Medicine in Baltimore. "These genetic factors are believed to be good probes to explore mechanistic links between brain development and adult brain functions."
Dr. Sawa, coauthor Dr. Toshitaka Nabeshima from the Department of Clinical Pharmacology at Meijo University in Nagoya, Japan, and their colleagues showed that a transient reduction of one of the susceptibility genes linked with schizophrenia (Disrupted-in-Schizophrenia-1) in the mouse prefrontal cortex just before or after birth led to aberrant changes in adult animals that are associated with schizophrenia, including perturbation of specific dopaminergic brain pathways, disruption of neural circuitry, and severe behavioral abnormalities.