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Insights into Dopamine Dysfunction

Dr Tertia Purves-Tyson is leading a research progam in NeuRA’s Schizophrenia Research Laboratory which is aimed at gaining greater insights into the behavior of dopamine.

“While there are many roads leading to the development of schizophrenia, one often considered a final common pathway is the dysregulation of dopamine. Too much dopamine in a particular region of the brain – the subcortex – has been shown to contribute to the psychotic symptoms seen in schizophrenia” – Says Dr Purves-Tyson

Dopamine is a neurotransmitter which helps to control the brain’s reward and pleasure centre, and regulates our emotions. Antipsychotics are designed to block dopamine receptors, and reduce the amount of dopamine action in the brain. Unfortunately, antipsychotics do not work for everyone and have serious side e€ffects.

A better understanding of how and where dopamine is changed in the brains of people with schizophrenia will help us to know how to more accurately correct or prevent this disruption and thus help to create more targeted approaches to treatment.

A new study from Dr Purves-Tyson and her team in the Schizophrenia Research Laboratory identified molecular changes in the brains of people with schizophrenia, which offers support for and extends the dopamine hypothesis. Their study compared the tissues from the midbrain of people with and without schizophrenia.

This brain region has not previously been given the attention it deserves in schizophrenia research. The study found that the genes of molecules which are responsible for regulating the amount of dopamine and for regulating the reaction to dopamine (receptors) are altered in people with schizophrenia.

These alterations in gene expression implicate a new suspect as a major contributor to dopamine dysregulation, namely a massive decrease in a dopamine transporter. The 66 percent reduction in this important molecule would mean that dopamine may be allowed to stay in the synapse longer than it should and suggests that novel treatments aimed at ramping up the synthesis and function of this process in schizophrenia could be of benefit. To our knowledge, the dopamine transporter has not been used as a treatment target before.

This study begins to address a vital knowledge gap in schizophrenia research with regards to how dopamine in the midbrain contributes to dopamine dysfunction. This will help us to better understand the dopamine dysregulation that is found in schizophrenia and, potentially, how we can better treat it.