For many people with post-traumatic stress disorder (PTSD), the most difficult part of recovery is not the initial trauma — it’s the way the brain keeps replaying those fearful memories, even when the danger is long gone.
This inability to “switch off” fear has puzzled scientists for decades and made treatment a major challenge. Current medicines, which mostly target serotonin in the brain, help only a small number of patients and often provide limited relief.
Now, researchers from the Institute for Basic Science (IBS) in South Korea and Ewha Womans University have found a new explanation for why the brain clings to these fear memories — and they’ve identified a drug that could help people finally let them go.
The research team, led by Dr. C. Justin Lee and Professor Lyoo In Kyoon, discovered that certain brain support cells called astrocytes play a surprising role in PTSD. Astrocytes are star-shaped cells that help maintain the brain’s environment.
In PTSD, these cells were found to produce too much of a brain chemical called GABA (gamma-aminobutyric acid). Normally, GABA calms overactive brain activity, but too much of it in the wrong place can shut down brain circuits that are needed to erase fear memories.
The researchers focused on a brain region called the medial prefrontal cortex (mPFC), which helps control fear and regulate emotions.
Brain scans of more than 380 people showed that PTSD patients had unusually high levels of GABA in this area and lower blood flow compared to healthy individuals. When some patients improved after treatment, their GABA levels dropped — a strong sign that excess GABA was connected to recovery.
To find out where this extra GABA was coming from, the scientists studied brain tissue from people who had died and used PTSD-like mouse models.
They discovered that the culprit was not the brain’s nerve cells (neurons), but astrocytes producing too much GABA through an enzyme called monoamine oxidase B (MAOB). This “astrocytic GABA” was dampening brain activity, making it almost impossible for the brain to unlearn fear.
The team then tested a drug called KDS2010, which was developed at IBS to block MAOB. This drug is special because it can cross into the brain and selectively stop astrocytes from making too much GABA.
When given to mice with PTSD-like symptoms, KDS2010 lowered GABA levels, improved blood flow in the mPFC, and — most importantly — allowed the mice to forget their fear responses. The drug restored the brain’s normal ability to erase traumatic memories.
What makes this discovery even more exciting is that KDS2010 has already passed early safety tests (Phase 1 trials) in humans and is currently in Phase 2 trials. That means it’s already on the path toward possible clinical use.
The study is also notable for its “reverse translational” approach. Instead of starting in the lab and moving to human testing, the researchers began with brain scan results from PTSD patients, traced the problem back to astrocytes, and then confirmed the mechanism in mice. This helped bridge the gap between human symptoms and basic brain biology.
“This is the first time astrocyte-derived GABA has been identified as a key cause of fear extinction problems in PTSD,” said Dr. Won Woojin, co-first author of the study. “Our results open the door to a completely new kind of treatment.”
If further testing is successful, KDS2010 could represent a major shift in PTSD therapy — moving away from traditional serotonin-based drugs toward treatments that directly target brain support cells.
The findings could also have broader benefits for other mental health conditions, including panic disorder, depression, and schizophrenia, where similar brain mechanisms might be involved.
This study is groundbreaking because it shifts the focus of PTSD research from neurons to astrocytes — a type of brain cell long thought to be just “support staff” for neurons. By showing that astrocytes can actively contribute to psychiatric symptoms, the researchers have opened a new path for treatment.
The discovery that blocking excess astrocytic GABA production can restore the brain’s ability to forget fear is especially important for patients who haven’t responded to current treatments.
With KDS2010 already moving through clinical trials, this approach could reach patients faster than most new drug discoveries. While more research is needed, especially in human PTSD patients, the work offers real hope for more effective therapies in the near future.
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The study is published in Signal Transduction and Targeted Therapy.
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