Whereas the exact causes of schizophrenia are unknown, abnormal neural developmental is a strong risk factor. The Szele group examine this relationship with human induced pluripotential stem cells (hIPSC), post-mortem human histology and a mouse model and find the three approaches indicate neurodevelopment is altered in schizophrenia. Our hIPSC data, generated in collaboration with Tony James and international colleagues indicate that mTOR signalling is significantly disrupted in schizophrenia. Histological examination of the caudate nucleus showed a significant decrease in calretinin+ cells in the disease. Finally, our dysbindin mutation x inflammation mouse model had disrupted neural stem cell niches.
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