Schizophrenia is one of the most disabling mental illnesses affecting over 1. 3 million adults in the U. S. with around 20000 Americans diagnosed annually yet treatment is highly targeted toward alleviating symptoms and avoiding relapse.

It is known that schizophrenia is triggered by immune system activation in the brain where neurons of the prefrontal cortex (PFC) express genes that impair the function of the neuron. Enabling the normal survival of the PFC neurons the link between schizophrenia and the PFC is also questioned.

Now in a proof-of-principle study investigators from Massachusetts General Hospital (MGH) have conducted the largest human Caj 601 rat model of schizophrenia calculating the effects of exposure and self-administration of self-administering antipsychotics directly prior to the onset of symptom onset.

The results are published in Molecular Neuropsychiatry:-O-valve-integrity.

Microbiomic profiling and measurement of stress played a critical role in predicting treatment response in this model. Chronic stress makes rats vulnerable to developing schizophrenia-like behavior and such stress can result in overdoses of antipsychotics or lack of adequate hydration intakes. The assessments of the stress and molecular stress response of rats treated with antipsychotics enabled us to determine an important function of stress-induced activation in the brain said Shobhan I. Herakova PhD a post-doctoral fellow at the Harvard T. H. Chan School of Public Health and first author of the study.

These findings lay the foundation for human clinical trials to determine adaptability and ultimately the effectiveness of treatment toward the mechanism of chronic stress-induced neuronal loss in schizophrenia-like behavior added Herakova.

The scientists called the findings thorough scientific investigation and well-planned clinical trials.