Schizophrenia in the Brain Blog #5

 

Angelina Tadros

November 26, 2025

Dr. Barbato

Genetics Blog #5

Schizophrenia in the Brain

A recent study aimed to map the genetic structure of schizophrenia in the brain, focusing on the caudate nucleus, an area linked to the disorder and targeted by antipsychotic medications. Researchers in this study analyzed postmorton tissue (which is biological tissue collected after a person has died) from 443 donors, including people with schizophrenia or bipolar disorder and healthy controls. They examined gene expression, identifying the risk genes, gene networks and how antipsychotic use influences brain activity. They found altered expression in over 2,700 genes in people with schizophrenia, revealing both known and new genes associated with the disorder. 

This study highlights the role of dopamine regulation in schizophrenia, specifically through the dopamine receptor gene DRD2. Reduced expression of this receptor in the caudate nucleus can lead to elevated dopamine levels, which are linked to symptoms like psychosis. Additionally, researchers used a new method to map gene networks, finding linked genes involved in neuron development and signaling. These findings reflect that schizophrenia and things like medication use can cause small changes in brain cells, which may lead to problems in thinking and behavior. Understanding these networks can help researchers make treatments that target multiple genes and biological pathways at the same time. Structural imaging studies have also shown that people at high risk for developing psychosis (converters), as well as people with schizophrenia, experience fast shrinking of certain brain regions, especially the prefrontal cortex, compared with nonconverters and healthy individuals (shown in Figure 1). These studies demonstrate how genetic and cellular changes in the brain can lead to obvious structural changes that may cause symptoms of schizophrenia.

Figure 1.

Converters: people at ultra high risk for psychosis who went on to develop psychosis.

Nonconverters: people at ultra high risk who did not develop psychosis.

Schizophrenia patients vs. healthy controls: Another comparison showing how brain contraction differs between diagnosed patients and healthy people.

Brain surface contraction: Red/pink areas on the scans show areas where the brain surface is shrinking faster over time, measured in mm/year. Blue areas show movement or growth, but the focus is on the contraction.

Prefrontal cortex: Both converters and schizophrenia patients show the most contraction as shown in figure 1, this ultimately affects functions like judgment, decision-making and impulse control.

This research has highlighted the complexity of genetic risk in schizophrenia and the importance of focusing on how genes work together in networks rather than in isolation. It also shows that treatments like antipsychotics have effects on gene expression and their effects should be considered in more genetic studies. Focusing on genetic networks could help professionals to develop treatments specific to a person's genetic needs, and possibly creating better treatments to help those living with schizophrenia. 

Sources

Article: https://www.nimh.nih.gov/news/science-updates/2022/researchers-map-the-genetic-landscape-of-schizophrenia-in-the-brain

Picture+other source: https://pmc.ncbi.nlm.nih.gov/articles/PMC4235761/

Are obese tendencies controled by gene variants?

A study presented during Obesity Week by researchers at the Imperial College London suggest they have found a pair of genetic variants that seem to correlate with obesity, as a result of increased reward responses in the brain to foods high in sugar and fat.  These two variants are located in the FTO gene and the DRD2 gene which are associated with risk of obesity.

The study found that activity in the striatum is increased in individuals with the FTO variant when looking at high calorie foods, this is only seen in those with a certain DRD2 variant, meaning that DRD2 variants have an effect on the dopamine system.

As a result of their findings the researchers suggest that individuals with FTO variants as well as DRD2 variants are more likely to be obese as a consequence to their altered dopamine signals, which cause them to have increased cravings for high calorie foods.

I find this to be quite interesting, because these results can possibly give some explanations as to why there are individuals who just struggle with being overweight, where the usual weight lose interventions don't exactly help.  Now that we know there could be some type of gene variation behind these behaviors, better more efficient "treatment" plans can be put into place, and maybe even some medications can be made/discovered to help these people who struggle with being overweight and constantly craving foods that are not good for them and causing their weight gain.

Original article

Study Finds Some People are 'Hard-Wired' to Prefer High Calorie Foods

Study leader Dr. Tony Goldstone, from Imperial College London in the UK, and colleagues have identified two genetic variants that influence whether we opt for high-calorie or low-calorie foods - a finding that that could open the door to more personalized treatment options for obesity. Dr. Goldstone and his colleagues set out to determine whether a person's food choices may be influenced by certain genetic variants. They conducted DNA genotyping on 45 European adults aged 19-55 to identify the presence of variants near two genes: the FTO gene, which has been associated with obesity predisposition, and the DRD2 gene, which plays a role in the regulation of dopamine in the brain. The subjects had a body mass index (BMI) ranging from 19 kg to 53.1 kg. Those subjects were asked to view pictures high and low-calorie foods and rate how appealing they were, while the researchers used functional magnetic resonance imaging (fMRI) to view brain activity.

They found that the participants who possessed a variant near the FTO gene and who rated the high calorie foods as more appealing demonstrated greater activity in a part of the brain called the orbitofrontal cortex. Based on their findings, the researchers suggest that individuals who possess the FTO gene may be at greater risk for obesity because dopamine signals trigger a sense of craving and reward in the presence of unhealthy foods. Dr. Goldstone says "It means they may experience more cravings than the average person when presented with high-calorie foods leading them to eat more of these foods." The study team suggests using gut hormones that target dopamine cells in the brain to alter the hormone's influence on cravings for high-calorie foods.

Obesity, basically, means having to much body fat and is different from overweight, which means weighing too much. Obesity occurs when over time when you eat more calories than you use. From this study, the team suggests that people who have the FTO gene may have a risk for obesity because of the dopamine triggers a sense of craving. This is very interesting because I had no idea obesity could be traced to the genetic level. This finding could be very beneficial to more treatments in the future, and may help stop obesity. More than a third of adults in the US, 78.6 million people, are obese and this study could help bring that number down because obesity can lead to heart disease, type 2 diabetes, and many more harmful diseases. This study helped me open my eyes about what foods to eat.

Original article here