Post-traumatic stress disorder, or PTSD, is a serious mental health condition that affects millions of people worldwide.
It often develops after someone has gone through a deeply frightening or life-threatening event such as war, natural disasters, violence, or severe accidents.
One of the biggest struggles for people with PTSD is that they cannot easily forget the traumatic memories, even when the actual danger is long gone.
The brain seems to hold on tightly to fear, and this constant replay of trauma makes it difficult to recover.
Scientists have long known that fear memories usually fade over time through a process called “fear extinction.” This is the brain’s way of learning that a once-dangerous situation is now safe. But in PTSD, this natural forgetting process does not work properly.
Current treatments, including medicines that target serotonin (the “feel good” chemical in the brain), only help some patients and often give only partial relief. This has left doctors and researchers searching for new answers.
A new study from the Institute for Basic Science (IBS) and Ewha Womans University in South Korea has revealed an unexpected brain mechanism that may explain why PTSD symptoms are so persistent.
The team, led by Dr. C. Justin Lee and Professor Lyoo In Kyoon, discovered that star-shaped brain support cells called astrocytes produce too much of a chemical messenger known as GABA.
Normally, GABA helps calm the brain, but when there is too much of it in the wrong place, it can block the brain’s ability to “unlearn” fear. This imbalance prevents fear memories from fading, which is a hallmark of PTSD.
The researchers focused on the medial prefrontal cortex, a brain region that plays a key role in controlling fear and decision-making. Using brain imaging in more than 380 people, they found that PTSD patients had higher levels of GABA and reduced blood flow in this area.
Interestingly, patients who started to recover showed lower GABA levels, suggesting that controlling this chemical could be critical for healing.
To understand where the extra GABA came from, the team studied brain tissue from people with PTSD as well as mouse models of the disorder. They found that the source was astrocytes, not neurons. The culprit was an enzyme called monoamine oxidase B (MAOB), which drives abnormal GABA production.
Here comes the breakthrough: the team tested a drug called KDS2010, which blocks MAOB activity. The drug reduced GABA levels, restored normal brain activity, improved blood flow in the medial prefrontal cortex, and most importantly, allowed mice to forget fear responses.
This means the brain could finally let go of the traumatic memories. KDS2010 is already known to be safe in humans, having passed Phase 1 clinical trials, and is currently being tested in Phase 2.
What makes this research unique is the way the scientists worked backwards. They began with human brain scans to spot the problem, then traced it down to cells and molecules in the lab. This “reverse translational” method connected big-picture clinical findings with small-scale biology.
It also challenges the old idea that glial cells like astrocytes are just passive helpers. Instead, this study shows they play an active role in shaping mental health and psychiatric disorders.
The discovery is important for several reasons. First, it identifies astrocytic GABA as a key driver of PTSD symptoms. Second, it provides strong evidence that blocking MAOB with drugs like KDS2010 may help treat PTSD.
Third, it opens doors to treating other conditions, including panic disorder, depression, and schizophrenia, where similar brain mechanisms may be at play.
In conclusion, this study shines a new light on how PTSD develops and why it is so hard to treat. It suggests that targeting astrocytes and their abnormal GABA production could become a completely new way to help patients who do not benefit from current therapies.
While more research is needed, especially in larger human trials, this discovery represents real hope for the future of PTSD treatment.
The study is published in Signal Transduction and Targeted Therapy.
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