Groundbreaking Discovery Offers Hope for PTSD Patients

For decades, patients suffering from post-traumatic stress disorder (PTSD) have struggled to forget traumatic memories, even after the danger has passed. The failure to extinguish these fear memories has long puzzled scientists and presented a significant hurdle in treatment, particularly since current medications targeting serotonin receptors offer limited relief for only a subset of patients.

A recent discovery by researchers at the Institute for Basic Science (IBS) and Ewha Womans University has uncovered a new brain mechanism driving PTSD. Led by Dr. C. Justin LEE at the IBS Center for Cognition and Sociality and Professor LYOO In Kyoon at Ewha Womans University, the team found that excessive GABA produced by astrocytes impairs the brain’s ability to extinguish fear memories. This deficit is a core feature of PTSD, explaining why traumatic memories can persist long after the threat has passed.

The researchers discovered that a highly selective and reversible monoamine oxidase B (MAOB) inhibitor called KDS2010 can reverse PTSD-like symptoms in mice. The drug has already passed Phase 1 safety trials in humans, making it a strong candidate for future PTSD treatments.

PTSD remains challenging to treat, with current medications targeting serotonin pathways providing limited relief for many patients. The new study focused on the medial prefrontal cortex (mPFC), a region of the brain critical for regulating fear. Importantly, GABA levels decreased in patients who showed clinical improvement, highlighting the chemical’s central role in recovery.

To uncover the origin of this excess GABA, the researchers examined postmortem human brain tissue and used PTSD-like mouse models. They found that astrocytes were producing abnormal amounts of GABA via the enzyme monoamine oxidase B (MAOB). This astrocyte-derived GABA impaired neural activity, blocking the brain’s ability to forget traumatic memories.

When KDS2010 was administered to mice, they showed normalized brain activity and were able to extinguish fear responses. The drug reduced GABA levels, restored blood flow in the mPFC, and re-enabled memory extinction mechanisms. This study confirms astrocytic MAOB as a central driver of PTSD symptoms and MAOB inhibition as a viable therapeutic path.

A major challenge was linking clinical findings in humans with cellular mechanisms in the lab. The researchers applied a “reverse translational” strategy: they began with clinical brain scans, moved backward to identify the cellular source of dysfunction, then confirmed the mechanism and tested drug effects in animal models. This approach led to a new understanding of how glial cells actively shape psychiatric symptoms.

“This study is the first to identify astrocyte-derived GABA as a key pathological driver of fear extinction deficit in PTSD,” said Dr. WON Woojin, a postdoctoral researcher and co-first author of the study. “Our findings not only uncover a novel astrocyte-based mechanism underlying PTSD but also provide preclinical evidence for a new therapeutic approach using an MAOB inhibitor.”
Director C. Justin LEE emphasized that “This work represents a successful example of reverse translational research, where clinical findings in humans guided the discovery of underlying mechanisms in animal models. By identifying astrocytic GABA as a pathological driver in PTSD and targeting it via MAOB inhibition, the study opens a completely new therapeutic paradigm not only for PTSD but also for other neuropsychiatric disorders such as panic disorder, depression, and schizophrenia.”
The researchers plan to further investigate astrocyte-targeted therapies for various neuropsychiatric disorders. With KDS2010 currently undergoing Phase 2 clinical trials, this discovery may soon lead to new options for patients whose symptoms have not responded to conventional treatments.

The COVID-19 pandemic has left an indelible mark on humanity, but its impact may go beyond the physical toll of the virus itself. A recent study suggests that even those who never contracted COVID-19 may have experienced accelerated brain aging due to the stresses and disruptions caused by the pandemic.

Led by experts at the University of Nottingham, the research team analyzed longitudinal brain scans from nearly 1,000 healthy adults, taken as part of the UK Biobank study. Some participants had scans before and after the pandemic, while others only had pre-pandemic scans. Using advanced imaging and machine learning, the researchers estimated each person’s “brain age” – how old their brain appeared to be compared to their actual age.

The findings were striking: people who lived through the pandemic showed signs of faster brain aging over time than those scanned entirely before it. The changes were most noticeable in older individuals, men, and those from more disadvantaged backgrounds. Notably, only participants who were infected with COVID-19 between their scans showed a drop in certain cognitive abilities, such as mental flexibility and processing speed.

“This study reminds us that brain health is shaped not only by illness but by our everyday environment,” said Dorothee Auer, Professor of Neuroimaging and senior author on the study. “The pandemic put a strain on people’s lives, especially those already facing disadvantage. We can’t yet test whether the changes we saw will reverse, but it’s certainly possible, and that’s an encouraging thought.”

Stress, isolation, and global disruption may have left their mark on people’s minds, leading to accelerated brain aging. However, the study highlights the possibility of reversibility, offering a glimmer of hope for those affected. The pandemic has taught us that even in the face of adversity, our brains can adapt and potentially recover – a testament to the resilience of the human spirit.

Are you struggling to sleep at night, feeling restless and unfocused during the day? Do you find it hard to concentrate on tasks or activities that normally bring you joy? You’re not alone. Research suggests that adults with Attention Deficit Hyperactivity Disorder (ADHD) traits are more likely to experience insomnia, which can exacerbate their symptoms.

A recent study published in BMJ Mental Health found a strong link between ADHD traits, insomnia severity, and reduced life satisfaction. The researchers analyzed data from over 1,300 adult participants who completed an online survey about ADHD traits, sleep disturbances, circadian factors, depression, and quality of life. Their findings revealed that:

* Adults with higher ADHD traits reported worse depression, more severe insomnia, lower sleep quality, and a preference for going to bed and waking up later.
* Insomnia severity predicted a lower quality of life, suggesting that it may be a key factor in the vicious cycle between ADHD and reduced well-being.

The study’s lead author, Dr. Sarah L. Chellappa, notes that “sleep disruption can impact neurobehavioral and cognitive systems, including attention and emotional regulation.” This underscores the importance of addressing insomnia in individuals with ADHD traits.

Professor Samuele Cortese, a co-author on the paper, emphasizes the need for further research to understand this complex interplay between ADHD and insomnia. He suggests that targeting insomnia complaints through therapies like Cognitive Behavioral Therapy for Insomnia (CBT-I) or Sleep Restriction therapy may help improve the quality of life for individuals with higher ADHD traits.

While the study’s findings are promising, it’s essential to remember that every individual is unique, and addressing insomnia requires a personalized approach. By acknowledging the intersection of ADHD and insomnia, we can begin to break this vicious cycle and work towards improving overall well-being.

If you or someone you know struggles with ADHD and insomnia, consider consulting a healthcare professional for guidance on managing symptoms and improving quality of life.