When most people hear about autism spectrum disorder (ASD), they think of the core features—difficulties with social communication, challenges in interpreting cues, and the repetitive behaviors that often define the diagnosis. Yet autism is far more complex than these widely recognized traits. Hidden beneath the surface lies another struggle that many individuals with ASD face: anxiety.
Nearly 40% of children with autism also experience clinically significant anxiety disorders. These children often react with unusually strong fear responses, sometimes holding onto frightening experiences far longer than their peers. For some, this vulnerability resembles post-traumatic stress disorder (PTSD), with its hallmark symptom of being unable to escape the grip of painful memories. Until recently, however, this resemblance was largely anecdotal. Scientists lacked a clear understanding of what was happening in the brain to cause such lasting fear.
Now, groundbreaking research has begun to connect the dots, offering the first detailed explanation of why autism can increase susceptibility to trauma.
The Fear That Doesn’t Fade
At the heart of trauma is the inability to let go of fear. In typical brains, when something terrifying happens—a loud crash, a painful fall, a violent experience—the memory forms quickly and powerfully. But with time and repeated safe experiences, the brain gradually extinguishes the fear response. The next time you hear a loud crash, you may still jump, but your body learns to recognize that it does not always signal danger.
For many individuals with autism, this process appears broken. Fear does not fade. Instead, it lingers, replaying with the same intensity long after the original event has passed. Scientists have long wondered whether this reflects a deeper dysfunction in the brain’s fear circuits.
A recent study led by Professor Kim Eunjoon at the Institute for Basic Science (IBS) in South Korea has now illuminated the biological underpinnings of this phenomenon. The team’s work, published in Science Advances, reveals how a genetic mutation linked to autism disrupts the brain’s ability to erase fear, locking traumatic memories in place.
A Gene at the Center of Trauma
The study focused on a gene called Grin2b, which encodes a protein known as GluN2B. This protein is part of NMDA receptors, molecular gatekeepers that regulate how neurons communicate and adapt in response to experience. Mutations in Grin2b have long been associated with autism, but their role in shaping trauma responses remained unclear.
To investigate, researchers used mice engineered to carry a human ASD-linked mutation in Grin2b. These mice could learn fear normally—they froze when exposed to a frightening stimulus, just like their healthy counterparts. But when it came time to extinguish that fear, their brains refused to let go. Long after the danger was gone, the animals remained locked in states of heightened fear, resembling the prolonged, intrusive responses seen in PTSD.
The scientists discovered why: in these mutant mice, a key brain region called the basal amygdala (BA)—a hub for fear learning and extinction—became abnormally silent after trauma. Instead of helping the brain unlearn danger, the BA shut down, leaving fear memories fixed in place.
The Silent Amygdala
The amygdala has long been known as the brain’s “fear center,” but this research revealed something unexpected: silence, not overactivity, was the problem. Using electrophysiological recordings, the team found that excitatory neurons in the basal amygdala displayed suppressed synaptic activity after trauma. In other words, the very neurons needed to overwrite fear memories had gone quiet.
“ These animals could learn fear just fine, but they couldn’t unlearn it,” explained Professor Kim. “The amygdala essentially shut down when it was needed most, leaving the traumatic memory locked in place.”
This insight reframes how scientists think about trauma in autism. Rather than being overly sensitive to fear, individuals with ASD may instead struggle with the extinction of fear, making them vulnerable to PTSD-like patterns.
Reawakening Fear Circuits
If the amygdala’s silence is the problem, could reactivating it be the solution? The team set out to test this bold idea. Using a technique called chemogenetics, they selectively stimulated the BA neurons during fear-extinction training. The results were remarkable.
Once reactivated, the amygdala’s excitatory neurons began firing normally again. The mice were suddenly able to extinguish fear responses, behaving much like non-mutant mice. The exaggerated long-term fear that had gripped them was released.
“This was the most exciting part of our study,” said co-first author Kang Muwon. “By reactivating those neurons, we could reverse both the behavioral and physiological abnormalities. It shows that these PTSD-like symptoms are not fixed—they can be changed.”
Building Bridges Between Autism and PTSD
This study represents more than a technical advance. It provides a crucial bridge between lived experiences and neuroscience. For years, families and clinicians have observed that people with autism seem especially vulnerable to trauma. Now, there is a clear biological explanation: a genetic mutation that silences the amygdala after trauma, preventing the brain from erasing fear.
The implications extend beyond autism. Understanding how the brain fails to extinguish fear could inform new therapies for PTSD itself, which affects millions of people worldwide. If reactivating silenced fear circuits can restore resilience in mice, perhaps future treatments—whether drugs or brain-stimulation techniques—could offer hope for human patients as well.
The Road Ahead
The IBS team is far from finished. Their next steps involve digging deeper into the molecular changes within the amygdala. By combining transcriptomic and proteomic analyses, they hope to map how gene expression shifts in BA neurons after trauma. They also plan to test receptor-specific drugs that target GluN2B-containing NMDA receptors, searching for potential therapeutic pathways.
While these advances remain in the laboratory for now, the message is clear: the roots of trauma in autism are not just psychological but biological. And by unraveling these roots, science is edging closer to interventions that could ease suffering for countless individuals.
A New Understanding of Fear in Autism
Autism is often misunderstood through the lens of what people with the condition struggle with—communication, social connection, or repetitive behaviors. But this research highlights another dimension: how autistic brains process fear and trauma. For many individuals, the pain of an experience is not fleeting; it echoes, lingering far longer than anyone can see.
By showing that a genetic mutation can silence fear circuits and that this silence can be reversed, the new findings give both scientific clarity and human hope. They remind us that behind every statistic about autism and anxiety are real lives, shaped by invisible battles with fear.
Physics once taught us why apples fall, and astronomy revealed why planets move. Now neuroscience is beginning to explain why some memories never fade—and how they might, someday, be released.
More information: Muwon Kang et al, Grin2b-mutant mice exhibit heightened remote fear via suppressed extinction and chronic amygdalar synaptic and neuronal dysfunction, Science Advances (2025). DOI: 10.1126/sciadv.adr7691. www.science.org/doi/10.1126/sciadv.adr7691
