This past week, the Concordia Neurochemistry Class talked about the neurology behind Schizophrenia, which is a long-term, developmental mental disorder that involves a dissociation between thought, emotion, and behavior.
This dissociation leads to symptoms such as hallucinations, delusions, withdrawal from reality, and a sense of mental fragmentation.
Similar to Autism, the diagnosis of Schizophrenia lies on a spectrum. Some people are able to function well in society while having this disorder, and some are unable to. Those who are very low functioning often live in group homes or hospitals.
One of the topics we talked about during the Friday discussion was the treatment of Schizophrenia, and where we think the research should focus on. Being such a “reactive” instead of “proactive” mental-health system, a lot of the research and funding is going towards treating those who are currently diagnosed.
Some people agreed with that. It is—for obvious reasons—essential to help those who are already trapped by such an inhibiting disorder. It is important to make sure that they are receiving adequate care and have access to current antipsychotic medication.
However, we also talked about the importance of nipping it in the bud by focusing research on neurodevelopment and understanding how the brain develops and, therefore, what causes the malfunction in neural communication that leads to disorders such as Schizophrenia.
Right now, there is research on certain hypothesis and theories regarding Schizophrenia that may explain the cause of the symptoms of the disorder.
The oldest and most established is the Dopamine Hypothesis.
Dopamine is a neurotransmitter that is a precursor for adrenaline, and is part of the reward pathway in the brain. That means that it is the neurotransmitter that is released when something “feels good.”
The Dopamine (DA) Hypothesis started off as stating simply that there is an increased amount of Dopamine in the brain of someone with Schizophrenia. Now, thanks to Neuroimaging techniques and advanced research, the DA Hypothesis has even more support.
Studies since the ‘90s have been focused on pinpointing the exact impact that Dopamine has on Schizophrenia. Some had found that the most prominent Dopamine receptor is D1, and Dopamine is unable to properly bind to those receptors, causing an influx in DA in areas of the brain such as the prefrontal cortex, which would explain some of the cognitive symptoms of Schizophrenia such as inhibited working memory and attention deficits.
This influx of Dopamine then causes a misfiring in a signaling cascade, which leads to a lack of Dopamine in the mesolimbic system. This is correlated with the negative symptoms of Schizophrenia, which include social withdrawal, lack of emotion, and inability to experience pleasure.
Our increasing knowledge about Dopamine and Schizophrenia means that we have a potential explanation for Schizophrenia symptomology, but what’s next?
By encouraging research on development and the direct etiology of neurodevelopmental disorders such as Schizophrenia, we will be able to identify what causes the abnormal Dopamine amounts in the brain, and how we can better treat, prevent, and even cure this disorder.