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Disruptions to the brain's internal GPS can result in the severe memory deficits associated with schizophrenia, says a new study published in Nature Neuroscience earlier this month.

Schizophrenia is a mental disorder whose symptoms include paranoia, hallucinations, delutions, and severe memory deficits. Antipsychotic drugs are effective at treating the first three symptoms, but are ineffective at dealing with the memory deficits.

"It is well known that cognitive dysfunction is a core feature of schizophrenia. Deficits range from moderate to severe across several domains, including attention, working memory, episodic memory, and executive functions. These deficits pre-date the onset of psychosis, are typically stable throughout the course of the illness  and are consistently the best predictor of functional outcome for patients," the paper's co-senior author, Dr. Joseph Gogos, a neuroscientist at Columbia University‚Äôs Zuckerman Institute, explained to ALN.

Because of this, the researcher team wanted to better understand what happens in the brains of schizophrenic patients.

They began by investigating episodic memory, which can be impaired in cases of schizophrenia.

The researchers developed experiments that allowed them to record CA1 activity in laboratory mice that were genetically modified to mimic schizophrenia. CA1 is a brain region, located in the hippocampus, that plays a role in navigation in episodic memory. Previous research had indicated physical alterations to this brain region in schizophrenia patients.

The schizophrenic mice were placed on a treadmill under a high-resolution, two-photon microscope and were then exposed to a variety of sights, sounds, and smells. This tested the animals' ability to navigate a new environment, remember how to navigate in familiar areas, and adapt when environments were changed.

There were dramatic differences in behavior and cell activity between the schizophrenic mice and the control group.

Both groups were able to successfully navigate new environments, however the schizphrenic mice had greater difficulty remembering familiar environments and adapting when the environment was altered.

Additionally, the brains of the schizophrenic mice behaved differently. Place cells, which fired with increasingly intensity when the control mice approached familiar territory, did not shift in the brains of schizophrenic mice.

This lack of adaptability could reflect the mechanismsof memory deficit in schizophrenia, the scientists argued.

"Antipsychotics, the mainstay of pharmacotherapy in schizophrenia,  are for the most part ineffective in treating cognitive symptoms. Moreover, despite advances in genetics and imaging progress in the development of cognitive enhancing agents in schizophrenia has been relatively disappointing. Thus, it is a high priority to identify the biological underpinnings of cognitive deficits in schizophrenia and to develop effective treatments," Gogos concluded.

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