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Depression

Groundbreaking Discovery Offers Hope for PTSD Patients

Researchers discovered that PTSD may be driven by excess GABA from astrocytes, not neurons. This chemical imbalance disrupts the brain’s ability to forget fear. A new drug, KDS2010, reverses this effect in mice and is already in human trials. It could represent a game-changing therapy.

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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.

Depression

The Unseen Toll of the Pandemic: How Stress and Isolation May Be Aging Your Brain

Even people who never caught Covid-19 may have aged mentally faster during the pandemic, according to new brain scan research. This large UK study shows how the stress, isolation, and upheaval of lockdowns may have aged our brains, especially in older adults, men, and disadvantaged individuals. While infection itself impacted some thinking skills, even those who stayed virus-free showed signs of accelerated brain aging—possibly reversible. The study highlights how major life disruptions, not just illness, can reshape our mental health.

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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.

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ADD and ADHD

Breaking the Cycle: How ADHD and Insomnia Can Intersect to Affect Quality of Life

Struggling to sleep might be the hidden reason why adults with ADHD traits often feel less satisfied with life. New research reveals a strong link between insomnia and reduced well-being in people with ADHD symptoms, suggesting a vicious cycle where poor sleep worsens attention and emotional issues, and vice versa.

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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.

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Anxiety

The Why Behind Exercise Matters More Than You Think

Movement helps your mood, but it’s not one-size-fits-all. Exercising for fun, with friends, or in enjoyable settings brings greater mental health benefits than simply moving for chores or obligations. Researchers emphasize that context — who you’re with, why you’re exercising, and even the weather — can make or break the mood-boosting effects.

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The relationship between exercise and mental health has been widely researched, but a recent study from the University of Georgia suggests that it’s not just the physical movement itself that affects mental well-being. Instead, it’s the why, where, and how you exercise that makes all the difference.

Historically, research on physical activity has focused on the length and intensity of exercise sessions, with little attention paid to the context in which they take place. However, this approach may be oversimplifying the complex relationship between exercise and mental health. As co-author Patrick O’Connor explains, “The ‘dose’ of exercise has been the dominant way researchers have tried to understand how physical activity might influence mental health, while often ignoring whether those minutes were spent exercising with a friend or as part of a game.”

Leisure-time physical activity, such as going for a run, taking a yoga class, or biking for fun, has been shown to correlate with better mental health outcomes. However, these benefits may vary significantly depending on the environment and circumstances surrounding the activity. For example, exercising alone in a gym may have different effects than working out with friends in a park.

Multiple studies have found that people who engage in regular leisure-time physical activity tend to report lower levels of depression and anxiety. However, it’s less clear whether other forms of physical activity, such as cleaning the house or working for a lawn care company, have similar benefits.

The context of exercise can also play a significant role in its impact on mental health. As O’Connor notes, “If you do the exact same exercise but miss the goal and people are blaming you, you likely feel very differently.” This highlights the importance of considering not only the physical activity itself but also the social and emotional aspects surrounding it.

Randomized controlled trials have shown that adopting regular exercise routines can boost mental health, especially for individuals with existing mental health disorders. However, these studies were typically based on small, short-term, and homogenous samples, so their results may not be generalizable to larger, more diverse groups.

The average effects of exercise on mental health are small across all the randomized controlled studies, partly because most of them focused on people who were not depressed or anxious. This suggests that larger- and longer-term controlled studies are needed to make a compelling case for whether exercise does, or does not, truly impact mental health.

Ultimately, understanding contextual factors is crucial in determining the impact of exercise on mental health. As O’Connor concludes, “If we’re trying to help people’s mental health with exercise, then not only do we need to think about the dose and the mode, we also need to ask: What is the context?” By considering these factors, researchers can develop more effective strategies for promoting mental well-being through physical activity.

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