New Hope for PTSD Treatment: Scientists Discover Astrocytes as Hidden Culprit Behind Chronic Symptoms
Living with post-traumatic stress disorder (PTSD) can feel like being trapped in a perpetual state of alert. For those suffering from post-traumatic stress disorder chronic symptoms, finding effective treatment remains challenging. However, a groundbreaking study from South Korea may have identified a key pathological driver—and a promising new post-traumatic stress disorder treatment target.
The GABA Imbalance in PTSD
The prefrontal cortex (PFC), a brain region critical for fear regulation, often shows dysfunction in PTSD patients. Research has long suggested that an imbalance in GABA—a key inhibitory neurotransmitter—plays a role. Now, scientists from the Institute for Basic Science and Ewha Womans University have pinpointed exactly where this imbalance originates: star-shaped brain cells called astrocytes.
In individuals with post-traumatic stress disorder (PTSD), these astrocytes become overactive and produce excessive amounts of GABA through an enzyme called monoamine oxidase B (MAOB). This surplus of astrocyte-derived GABA disrupts normal brain circuit function, impairing the ability to suppress fear responses—a hallmark of both post-traumatic stress disorder acute and chronic forms.
From Human Data to Animal Models
The research team began by analyzing brain scans and GABA levels in human subjects. They found that individuals with ongoing post-traumatic stress disorder chronic symptoms had significantly higher prefrontal GABA levels and reduced cerebral blood flow compared to both healthy controls and those who had recovered from post-traumatic stress disorder acute episodes.
To confirm causality, they turned to mouse models. By genetically reducing MAOB in astrocytes, they reversed fear extinction deficits—a core PTSD-like behavior. Conversely, increasing MAOB in normal mice induced PTSD-like symptoms. This clear link highlights astrocytes’ central role in the disorder and opens new avenues for post-traumatic stress disorder treatment.
A Promising Drug Candidate: KDS2010
The team then tested a highly selective MAOB inhibitor called KDS2010 in PTSD-model mice. The results were striking: daily administration normalized GABA levels, restored cerebral blood flow, and significantly improved behavioral deficits. Importantly, KDS2010 has already completed Phase 1 trials in humans, showing good safety profiles.
This positions MAOB inhibition as a novel mechanism for post-traumatic stress disorder treatment, moving beyond traditional approaches that often offer limited relief.
What This Means for Future PTSD Treatment
This study shifts the focus from neurons to astrocytes, highlighting these cells as critical players in post-traumatic stress disorder (PTSD) pathology. For patients, especially those with post-traumatic stress disorder chronic symptoms resistant to current therapies, MAOB inhibitors like KDS2010 represent a beacon of hope. As clinical trials progress, this research could lead to the first astrocyte-targeted post-traumatic stress disorder treatment, fundamentally changing how we approach this debilitating condition.
Source:
Yoon S, et al. Astrocytic gamma-aminobutyric acid dysregulation as a therapeutic target for posttraumatic stress disorder. Signal Transduction and Targeted Therapy. 2025. doi:10.1038/s41392-025-02317-5
This article is for informational purposes only and does not constitute medical advice. Please consult a healthcare professional for any health concerns.