Inflammatory diseases, like rheumatoid arthritis, Crohn’s disease, and ulcerative colitis, are complex illnesses that can make people feel sick, even when they’re on medication.
What makes these diseases tricky is that they don’t look or act the same in every patient. In fact, these illnesses can even change in the same person over time.
These diseases work by changing the behavior of thousands of genes in different organs and cell types. Diagnosing and treating such varied and complex changes is a real challenge.
That’s why researchers at the Karolinska Institutet in Sweden decided to tackle the problem in a new way.
Using Digital Twins to Study Inflammatory Diseases
These researchers created “digital twins” or digital models of each patient’s unique disease mechanisms.
These models are essentially personalized computer simulations that help the researchers better understand the disease in each patient.
By studying these models, the research team discovered a possible solution: the disease changes could be sorted into groups called molecular programs.
Molecular programs are controlled by a limited number of proteins, which work like switches. Some of these “switch proteins” are known targets for drugs like TNF inhibitors. However, these treatments don’t work for everyone.
New Findings and Future Possibilities
“We found that different patients have different switch proteins,” said Mikael Benson, the researcher leading the study.
“Also, we discovered that these proteins don’t simply turn the diseases on or off. Instead, they act more like dimmer switches, increasing or decreasing the severity of the disease.”
In other words, the proteins don’t eliminate the disease, but rather adjust its intensity.
Every bodily process can be described with mathematical equations, and by analyzing each gene’s activity in thousands of individual cells, these equations can be adjusted to fit each patient’s unique condition.
This could predict the outcome if a condition changes, like changing the dose of a medication.
This research opens up new possibilities for treating serious diseases. “We can develop methods to create the right combination of drugs for the ‘on’ proteins in each patient,” said Dr. Benson.
“We will make our programs available to other researchers so they can conduct more studies on patients with different immune diseases.”
The researchers in this study used a combination of analyzing a mouse model of rheumatoid arthritis and digital twins of human patients with various inflammatory diseases.
“We found that even though only the joints were inflamed in the mice, thousands of genes changed their activity in different cell types in ten different organs,” says Dr. Benson.
“This is the first time we’ve been able to see such a broad picture of how many organs are affected in rheumatoid arthritis.”
This discovery is a significant step forward in understanding and treating complex inflammatory diseases.
With this knowledge, we could move toward more personalized drug therapies that could potentially be more effective and cause fewer side effects.
This is an exciting development that could significantly improve the quality of life for people with these conditions.
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The study was published in Cell Reports Medicine.
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