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Depression is Not Only a Disease of the Mind. KAIST Discovers the Immune-Brain Connection
<(From Left) Ph.D candidate Insook Ahn from KAIST, Professor Jinju Han from KAIST, (Upper Left) Yangsik Kim from Inhan University School of Medicine, Ph.D candidate Soyeon Chang(psychiatrist)>
Major depressive disorder (MDD) is characterized by a lowered mood and loss of interest, contributing not only to difficulties in academic and professional life but also as a major cause of suicide in South Korea. However, there are currently no objective biological markers that can be used for diagnosis or treatment. Amidst this, a research team from KAIST has revealed that depression is not merely a problem of the mind or brain, but is deeply connected to abnormalities in the body's overall immune response. They found that this immune abnormality affects brain function, and the 'Immune Neural Axis' imbalance is the core mechanism of depression, opening up the possibility for the discovery of new biomarkers and the development of new drugs for depression treatment.
KAIST announced on the November 20th that Professor Jinju Han's research team from the Graduate School of Medical Science and Engineering (GSMSE) at KAIST, in collaboration with Professor Yangsik Kim's research team (Ph.D., KAIST GSMSE) from Inha University School of Medicine, performed a multi-omics analysis combining plasma proteomic analysis, WBC single-cell analysis, and patient-derived brain organoids (mini-brains). This study focused on female patients with MDD who exhibited 'Atypical Features' (such as hypersomnia and overeating) and 'Psychotic Symptoms'(such as auditory hallucinations and idea of reference), which are different from typical depression symptoms, and who also had impaired reality judgment.
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■ "Immune Cells and Brain Function are Altered Together" A New Biological Clue for Depression
The research team simultaneously examined genetic changes in immune cells in the blood and changes in nervous-system-related proteins. The results confirmed a breakdown in the balance of immune-neural interaction in patients with depression.
MDD, especially in young women, often presents with atypical symptoms (hypersomnia, overeating, mood reactivity, etc.), which increases the risk of a later diagnosis of bipolar disorder. Furthermore, about 40% of patients are classified as treatment-resistant depression, showing no response to various antidepressants.
Consequently, there has been a continuous call for the development of new therapeutic strategies and the discovery of biomarkers based on immunity and metabolism, moving beyond the traditional drug-centric approach.
■ World's First Integration of "Leukocyte Single-Cell Analysis + Brain Organoid" A New Paradigm for Psychiatric Research
The research team presented the world's first precision medicine approach by integrating plasma proteomics, leukocyte single-cell transcriptome analysis, and analysis of brain organoids created from patient-derived induced pluripotent stem cells (iPSCs).
The results showed that patients with atypical depression exhibited high levels of stress, anxiety, and depression. Furthermore, proteins crucial for inter-neuronal signaling (DCLK3 and CALY) were significantly elevated compared to normal levels, and Complement Protein C5, which strongly enhances the body's immune response, was also increased. This indicates that both 'brain function' and 'immune function' are excessively activated and out of balance within the body.
This finding confirms a clue that depression is not merely a mood issue but is connected to biological changes occurring throughout the entire body. Upon examining the immune cells of depression patients, genetic changes were found that make inflammatory responses in the body occur more easily and strongly than usual. This implies that the entire bodily immune system is in a state of excessive activation, and this immune/inflammatory abnormality may influence the development of depression.
The patient-derived brain organoids showed accompanying growth retardation and abnormal neural development, supporting the possibility that immune abnormalities interact with changes in brain function to exacerbate the disease.
■ "Immune-Neural Axis Imbalance is the Core Mechanism of Atypical Depression"
This study integrated clinical data, single-cell omics, proteomics, and brain organoids to demonstrate that the 'Imbalance of the Immune-Neural Axis' is the core mechanism of MDD accompanied by atypical and psychotic symptoms.
<Integration of clinical symptoms, blood analysis, and patient-derived brain organoid analysis in women with major depressive disorder>
Professor Jinju Han stated, "This achievement presents a new precision medicine model for psychiatric research," adding, "We anticipate that this will actively lead to biomarker discovery and new drug development."
This accomplishment was published online in the world-renowned international scientific journal, Advanced Science, on October 31st.
※ Paper Title: Exploration of Novel Biomarkers through a Precision Medicine Approach Using Multi-omics and Brain Organoids in Patients with Atypical Depression and Psychotic Symptoms DOI: https://doi.org/10.1002/advs.202508383
※ Author Information: Soyeon Chang (Inha University, Co-First Author), Seok-Ho Choi, Jiyoung Lee, Yangsik Kim (Inha University, Corresponding Author), Insook Ahn (KAIST, Co-First Author), and Jinju Han (KAIST, Corresponding Author)
This research was supported by the National Research Foundation of Korea and the Korea Health Industry Development Institute.
2025.11.20 View 18303 -
Refrigerator Use Increases with Stress, IoT Sensors Read Mental Health
<(From Left) Ph.D candidate Chanhee Lee, Professor Uichin Lee, Professor Hyunsoo Lee, Ph.D candidate Youngji Koh from School of Computing>
The number of single-person households in South Korea has exceeded 8 million, accounting for 36% of the total, marking an all-time high. A Seoul Metropolitan Government survey found that 62% of single-person households experience 'loneliness', deepening feelings of isolation and mental health issues. KAIST researchers have gone beyond the limitations of smartphones and wearables, utilizing in-home IoT data to reveal that a disruption in daily rhythm is a key indicator of worsening mental health. This research is expected to lay the foundation for developing personalized mental healthcare management systems.
KAIST (President Kwang Hyung Lee) announced on the 21st of October that a research team led by Professor Uichin Lee from the School of Computing has demonstrated the possibility of accurately tracking an individual's mental health status using in-home Internet of Things (IoT) sensor data.
Consistent self-monitoring is important for mental health management, but existing smartphone- or wearable-based tracking methods have the limitation of data loss when the user is not wearing or carrying the device inside the home.
The research team therefore focused on in-home environmental data. A 4-week pilot study was conducted on 20 young single-person households, installing appliances, sleep mats, motion sensors, and other devices to collect IoT data, which was then analyzed along with smartphone and wearable data.
The results confirmed that utilizing IoT data alongside existing methods allows for a significantly more accurate capture of changes in mental health. For instance, reduced sleep time was closely linked to increased levels of depression, anxiety, and stress, and increased indoor temperature also showed a correlation with anxiety and depression.
<Picture1. Heatmap of the Correlation Between Each User’s Mental Health Status and Sensor Data>
Participants' behavioral patterns varied, including a 'binge-eating type' with increased refrigerator use during stress and a 'lethargic type' with a sharp decrease in activity. However, a common trend clearly emerged: mental health deteriorated as daily routines became more irregular.
Variability in daily patterns was confirmed to be a more important factor than the frequency of specific behaviors, suggesting that a regular routine is essential for maintaining mental health.
When research participants viewed their life data through visualization software, they generally perceived the data as being genuinely helpful in understanding their mental health, rather than expressing concern about privacy invasion. This significantly enhanced the research acceptance and satisfaction with participation.
<Figure 2. Comparison of Average Mental Health Status Between the High Irregularity Group (Red) and the Low Irregularity Group (Blue)>
Professor Uichin Lee stated, "This research demonstrates that in-home IoT data can serve as an important clue for understanding mental health within the context of an individual's daily life," and added, "We plan to further develop this into a remote healthcare system that can predict individual lifestyle patterns and provide personalized coaching using AI."
Youngji Koh, a Ph.D candidate, participated as the first author in this research. The findings were published in the September issue of the Proceedings of the ACM on Interactive, Mobile, Wearable and Ubiquitous Technologies, a prominent international journal in the field of human-computer interaction (HCI). ※ Harnessing Home IoT for Self-tracking Emotional Wellbeing: Behavioral Patterns, Self-Reflection, and Privacy Concerns DOI: https://dl.acm.org/doi/10.1145/3749485 ※ Youngji Koh (KAIST, 1st author), Chanhee Lee (KAIST, 2nd author), Eunki Joung (KAIST, 3rd author), Hyunsoo Lee (KAIST, corresponding author), Uichin Lee (KAIST, corresponding author)
This research was conducted with support from the LG Electronics-KAIST Digital Healthcare Research Center and the National Research Foundation of Korea, funded by the government (Ministry of Science and ICT).
2025.10.21 View 2172 -
“Why are we depressed?” KAIST is identifying the cause of depression and uncovering clues for treatment
Major depressive disorder (MDD) is one of the most common psychiatric illnesses worldwide, but its molecular causes* have still not been clearly identified. A domestic research team has discovered that depression may not simply be caused by neuronal damage, but can also arise from the dysregulation of specific neural signaling pathways. In particular, they identified the molecular reason why elderly patients with depression do not respond to conventional antidepressants. This study suggests the possibility of therapeutic approaches using optogenetic technology to regulate neural signaling, and it provides clues for the development of new treatment strategies targeting the protein ‘Numb’ protein for elderly patients with depression.
*Molecular causes: explanations for the origin of a disease at the level of molecules, proteins, or genes in the brain.
KAIST (President Kwang Hyung Lee) announced on the 19th of August that a research team led by Distinguished Professor Won Do Heo of the Department of Biological Sciences at KAIST, in collaboration with forensic pathologist Minju Lee of the National Forensic Service (Director Bong Woo Lee) and Professor Seokhwi Kim of the Department of Pathology at Ajou University Medical Center (Director Sangwook Han), identified a new molecular mechanism for depression through RNA sequencing and the immunohistochemical analysis of brain tissue from patients who had committed suicide. Furthermore, they demonstrated in animal models that antidepressant effects can be restored by regulating the signaling pathway that induces neural recovery using optogenetic technology.
The research team focused on the hippocampus, the brain region responsible for memory and emotion, and in particular on the dentate gyrus (DG). The DG is the entry point of information into the hippocampus, playing a role in new memory formation, neurogenesis, and emotional regulation, and is closely linked with depression.
Using two representative mouse models for depression (the corticosterone stress model and the chronic unpredictable stress model), the team found that stress induced a striking increase in the signaling receptor FGFR1 (Fibroblast Growth Factor Receptor 1) in the DG. FGFR1 receives growth factor (FGF) signals and transmits growth and differentiation commands within cells.
Subsequently, using conditional knockout (cKO) mice in which the FGFR1 gene was deleted, the researchers revealed that the absence of FGFR1 made mice more vulnerable to stress and led them to exhibit depressive symptoms more quickly. This indicates that FGFR1 plays a critical role in proper neural regulation and stress resistance.
The team then developed an ‘optoFGFR1 system’ using optogenetics, enabling FGFR1 —essential for stress resistance—to be activated by light. They observed that activating FGFR1 in depression mouse models lacking FGFR1 restored antidepressant effects. In other words, they experimentally demonstrated that the activation of FGFR1 signaling alone could improve depressive behavior.
Surprisingly, however, in aged depression mouse models, the activation of FGFR1 signaling through the optoFGFR1 system did not yield antidepressant effects. Investigating further, the researchers found that in the aged brains, a protein called ‘Numb’ was excessively expressed and interfered with FGFR1 signaling.
Indeed, analysis of postmortem human brain tissue also showed the specific overexpression of Numb protein only in elderly patients with depression. When the researchers suppressed Numb using a gene regulatory tool (shRNA) while simultaneously activating FGFR1 signaling in mouse models, neurogenesis and behavior—previously unrecoverable—returned to normal even in aged depression models. This shows that the Numb protein acts as a “blocker” of FGFR1 signaling and is a key factor preventing the hippocampus from executing antidepressant mechanisms.
Distinguished Professor Won Do Heo of KAIST said, “This study is meaningful in that it revealed that depression may not only result from simple neuronal damage, but can also arise from the dysregulation of specific neural signaling pathways. In particular, we identified the molecular reason why antidepressants are less effective in elderly patients, and we expect this to provide a clue for the development of new therapeutic strategies targeting the Numb protein.”
He added, “Moreover, this interdisciplinary study, which combined KAIST’s expertise in neuroscience with the National Forensic Service’s forensic brain analysis technologies, is expected to serve as a bridge between basic research on psychiatric disorders and clinical applications.”
This study, led by first author Jongpil Shin, a PhD student in the Department of Biological Sciences at KAIST, was published on August 15, 2025, in the international journal Experimental & Molecular Medicine.
Paper title: “Dysregulation of FGFR1 signaling in the hippocampus facilitates depressive disorder”
DOI: https://doi.org/10.1038/s12276-025-01519-9
This research was supported by the Ministry of Science and ICT’s National Research Foundation of Korea through the ASTRA program and the Bio-Medical Technology Development project.
2025.08.19 View 2851 -
Decoding Fear: KAIST Identifies An Affective Brain Circuit Crucial for Fear Memory Formation by Non-nociceptive Threat Stimulus
Fear memories can form in the brain following exposure to threatening situations such as natural disasters, accidents, or violence. When these memories become excessive or distorted, they can lead to severe mental health disorders, including post-traumatic stress disorder (PTSD), anxiety disorders, and depression. However, the mechanisms underlying fear memory formation triggered by affective pain rather than direct physical pain have remained largely unexplored – until now.
A KAIST research team has identified, for the first time, a brain circuit specifically responsible for forming fear memories in the absence of physical pain, marking a significant advance in understanding how psychological distress is processed and drives fear memory formation in the brain. This discovery opens the door to the development of targeted treatments for trauma-related conditions by addressing the underlying neural pathways.
< Photo 1. (from left) Professor Jin-Hee Han, Dr. Junho Han and Ph.D. Candidate Boin Suh of the Department of Biological Sciences >
KAIST (President Kwang-Hyung Lee) announced on May 15th that the research team led by Professor Jin-Hee Han in the Department of Biological Sciences has identified the pIC-PBN circuit*, a key neural pathway involved in forming fear memories triggered by psychological threats in the absence of sensory pain. This groundbreaking work was conducted through experiments with mice.*pIC–PBN circuit: A newly identified descending neural pathway from the posterior insular cortex (pIC) to the parabrachial nucleus (PBN), specialized for transmitting psychological threat information.
Traditionally, the lateral parabrachial nucleus (PBN) has been recognized as a critical part of the ascending pain pathway, receiving pain signals from the spinal cord. However, this study reveals a previously unknown role for the PBN in processing fear induced by non-painful psychological stimuli, fundamentally changing our understanding of its function in the brain.
This work is considered the first experimental evidence that 'emotional distress' and 'physical pain' are processed through different neural circuits to form fear memories, making it a significant contribution to the field of neuroscience. It clearly demonstrates the existence of a dedicated pathway (pIC-PBN) for transmitting emotional distress.
The study's first author, Dr. Junho Han, shared the personal motivation behind this research: “Our dog, Lego, is afraid of motorcycles. He never actually crashed into one, but ever since having a traumatizing event of having a motorbike almost run into him, just hearing the sound now triggers a fearful response. Humans react similarly – even if you didn’t have a personal experience of being involved in an accident, a near-miss or exposure to alarming media can create lasting fear memories, which may eventually lead to PTSD.”
He continued, “Until now, fear memory research has mainly relied on experimental models involving physical pain. However, much of real-world human fears arise from psychological threats, rather than from direct physical harm. Despite this, little was known about the brain circuits responsible for processing these psychological threats that can drive fear memory formation.”
To investigate this, the research team developed a novel fear conditioning model that utilizes visual threat stimuli instead of electrical shocks. In this model, mice were exposed to a rapidly expanding visual disk on a ceiling screen, simulating the threat of an approaching predator. This approach allowed the team to demonstrate that fear memories can form in response to a non-nociceptive, psychological threat alone, without the need for physical pain.
< Figure 1. Artificial activation of the posterior insular cortex (pIC) to lateral parabrachial nucleus (PBN) neural circuit induces anxiety-like behaviors and fear memory formation in mice. >
Using advanced chemogenetic and optogenetic techniques, the team precisely controlled neuronal activity, revealing that the lateral parabrachial nucleus (PBN) is essential to form fear memories in response to visual threats. They further traced the origin of these signals to the posterior insular cortex (pIC), a region known to process negative emotions and pain, confirming a direct connection between the two areas.
The study also showed that inhibiting the pIC–PBN circuit significantly reduced fear memory formation in response to visual threats, without affecting innate fear responses or physical pain-based learning. Conversely, artificially activating this circuit alone was sufficient to drive fear memory formation, confirming its role as a key pathway for processing psychological threat information.
< Figure 2. Schematic diagram of brain neural circuits transmitting emotional & physical pain threat signals. Visual threat stimuli do not involve physical pain but can create an anxious state and form fear memory through the affective pain signaling pathway. >
Professor Jin-Hee Han commented, “This study lays an important foundation for understanding how emotional distress-based mental disorders, such as PTSD, panic disorder, and anxiety disorder, develop, and opens new possibilities for targeted treatment approaches.”
The findings, authored by Dr. Junho Han (first author), Ph.D. candidate Boin Suh (second author), and Dr. Jin-Hee Han (corresponding author) of the Department of Biological Sciences, were published online in the international journal Science Advances on May 9, 2025.※ Paper Title: A top-down insular cortex circuit crucial for non-nociceptive fear learning. Science Advances (https://doi.org/10.1101/2024.10.14.618356)※ Author Information: Junho Han (first author), Boin Suh (second author), and Jin-Hee Han (corresponding author)
This research was supported by grants from the National Research Foundation of Korea (NRF-2022M3E5E8081183 and NRF-2017M3C7A1031322).
2025.05.15 View 8799 -
A KAIST research team identifies a cause of mental diseases induced by childhood abuse
Childhood neglect and/or abuse can induce extreme stress that significantly changes neural networks and functions during growth. This can lead to mental illnesses, including depression and schizophrenia, but the exact mechanism and means to control it were yet to be discovered.
On August 1, a KAIST research team led by Professor Won-Suk Chung from the Department of Biological Sciences announced the identification of excessive synapse removal mediated by astrocytes as the cause of mental diseases induced by childhood abuse trauma. Their research was published in Immunity, a top international journal in the field of immunology.
The research team discovered that the excessive astrocyte-mediated removal of excitatory synapses in the brain in response to stress hormones is a cause of mental diseases induced by childhood neglect and abuse. Clinical data have previously shown that high levels of stress can lead to various mental diseases, but the exact mechanism has been unknown. The results of this research therefore are expected to be widely applied to the prevention and treatment of such diseases.
The research team clinically screened an FDA-approved drug to uncover the mechanism that regulates the phagocytotic role of astrocytes, in which they capture external substances and eliminate them. As a result, the team found that synthetic glucocorticoids, namely stress hormones, enhanced astrocyte-mediated phagocytosis to an abnormal level. Glucocorticoids play essential roles in processes that maintain life, such as carbohydrate metabolism and anti-inflammation, but are also secreted in response to external stimuli such as stress, allowing the body to respond appropriately. However, excessive and long-term exposure to glucocorticoids caused by chronic stress can lead to various mental diseases including depression, cognitive disorders, and anxiety.
< Figure 1. Results of screening for compounds that increase astrocyte phagocytosis
(A) Discovered that synthetic glucocorticoid (stress hormone) increases the phagocytosis of astrocytes through screening of FDA-approved clinical compounds. (B-C) When treated with stress hormones, the phagocytosis of astrocytes is greatly increased, but this phenomenon is strongly suppressed by the GR antagonist (Mifepristone). CORT: corticosterone (stress hormone), Eplerenone: mineralocorticoid receptor (MR) antagonist, Mifepristone: glucocorticoid receptor (GR) antagonist >
To understand the changes in astrocyte functions caused by childhood stress, the research team used mice models with early social deprivation, and discovered that stress hormones bind to the glucocorticoid receptors (GRs) of astrocytes. This significantly increased the expression of Mer tyrosine kinase (MERK), which plays an essential role in astrocyte phagocytosis. Surprisingly, out of the various neurons in the cerebral cortex, astrocytes would eliminate only the excitatory synapses of specific neurons. The team found that this builds abnormal neural networks, which can lead to complex behavioral abnormalities such as social deficiencies and depression in adulthood.
The team also observed that microglia, which also play an important role in cerebral immunity, did not contribute to synapse removal in the mice models with early social deprivation. This confirms that the response to stress hormones during childhood is specifically astrocyte-mediated.
To find out whether these results are also applicable in humans, the research team used a brain organoid grown from human-induced pluripotent stem cells to observe human responses to stress hormones. The team observed that the stress hormones induced astrocyte GRs and phagocyte activation in the human brain organoid as well, and confirmed that the astrocytes subsequently eliminated excessive amounts of excitatory synapses. By showing that mice and humans both showed the same synapse control mechanism in response to stress, the team suggested that this discovery is applicable to mental disorders in humans.
< Figure 2. A schematic diagram of the study published in Immunity. Excessive stress hormone secretion in childhood increases the expression of the MERTK phagocytic receptor through the glucocorticoid receptor (GR) of astrocytes, resulting in excessive elimination of excitatory synapses. Excessive synaptic elimination by astrocytes during brain development causes permanent damage to brain circuits, resulting in abnormal neural activity in the adult brain and psychiatric behaviors such as depression and anti-social tendencies. >
Prof. Won-Suk Chung said, “Until now, we did not know the exact mechanism for how childhood stress caused brain diseases. This research was the first to show that the excessive phagocytosis of astrocytes could be an important cause of such diseases.” He added, “In the future, controlling the immune response of astrocytes will be used as a fundamental target for understanding and treating brain diseases.”
This research, written by co-first authors Youkyeong Byun (Ph.D. candidate) and Nam-Shik Kim (post-doctoral associate) from the KAIST Department of Biological Sciences, was published in the internationally renowned journal Immunity, a sister magazine of Cell and one of the best journal in the field of immunology, on July 31 under the title "Stress induces behavioral abnormalities by increasing expression of phagocytic receptor MERTK in astrocytes to promote synapse phagocytosis."
This work was supported by a National Research Foundation of Korea grant, the Korea Health Industry Development Institute (KHIDI), and the Korea Dementia Research Center (KDRC).
2023.08.04 View 12163 -
KAIST Offers Hope to Musicians with Dystonia
< Photo 1. Conductor and Pianist João Carlos Martins before the Recital at the Carnegie Hall preparing with his bionic gloves >
KAIST’s neuroscientist and professor, Dr. Daesoo Kim attended the “Conference for Musicians with Dystonia” supported by the World Health Organization (WHO) and the Carnegie Hall concert of legendary pianist João Carlos Martins, who is also a dystonia patient, to announce his team’s recent advancements toward finding a cure for dystonia.
On November 19, 2022, a “miracle concert” was held in Carnegie Hall. João Carlos Martins was a renowned world-class pianist in the 70s and 80s, but he had to put an end to his musical career due to focal dystonia in his fingers. But in 2020, he began using a bionic glove developed by industrial designer Ubiratã Bizarro Costa and after years of hard work he was back in Carnegie Hall as an 82-year-old man.
During the concert, he conducted the NOVUS NY orchestra in a performance of Bach, and later even played the piano himself. In particular, between his performances, he gave shout-outs to scientists studying dystonia including KAIST Professor Daesoo Kim, asking them to continue working towards curing rare diseases for musicians.
< Photo 2. Professor Daesoo Kim with Conductor and Pianist João Carlos Martins >
Musician’s dystonia affects 1-3% of musicians around the world and musicians make up approximately 5% of the total number of dystonia patients. Musicians who are no longer able to practice music due to the disease often experience stress and depression, which may even lead to suicide in extreme cases. Musicians are known to be particularly prone to such diseases due to excessive practice regimens, perfectionism, and even genetics. Currently, botulinum toxin (Botox) is used to suppress abnormal muscles, but muscle function suppression ultimately means that the musician is no longer able to play the instrument. João Carlos Martins himself underwent several Botox procedures and three brain surgeries, but saw no therapeutic results. This is why a new treatment was necessary.
Professor Daesoo Kim’s research team at KAIST took note of the fact that abnormal muscle tension is caused by excessive stress, and developed NT-1, a treatment that blocks the development of the symptoms of dystonia from the brain, allowing patients to use their muscles as they normally would. The research team published their findings in Science Advances in 2021, and João Carlos Martins invited Professor Daesoo Kim to the UN conference and his concert after reading this paper.
< Photo 3. Professor Daesoo Kim (3rd from the left) photographed with other guests at the recital including Dr. Dévora Kestel, the Director of the Mental Health and Substance Use at WHO, sharing the center with Conductor and Pianist João Carlos Martins >
During the UN conference held the day prior to the Carnegie Hall concert, Dr. Dévora Kestel, Director of the Mental Health and Substance Use at WHO, said, “Although dystonia is not as well-known, it is a common disease around the world, and needs our society’s attention and the devotion of many researchers.” Professor Daesoo Kim said, “NT-1 is a drug that blocks the cause of dystonia in the brain, and will allow musicians to continue practicing music. We aim to attain clinical approval in Korea by 2024.”
NT-1 is currently under development by NeuroTobe, a faculty-led start-up company at KAIST, headed by Professor Daesoo Kim as the CEO. The synthesis of the drug for clinical testing has been successfully completed, and it has shown excellent efficacy and safety through various rounds of animal testing. Unlike Botox, which takes a few days to show its therapeutic effects after receiving the procedure from a hospital, NT-1 shows its therapeutic effects within an hour after taking it. As a so-called “edible Botox”, it is expected to help treat various muscular diseases and ailments.
2022.12.27 View 16864 -
Stress-Relief Substrate Helps OLED Stretch Two-Dimensionally
Highly functional and free-form displays are critical components to complete the technological prowess of wearable electronics, robotics, and human-machine interfaces.
A KAIST team created stretchable OLEDs (Organic Light-Emitting Diodes) that are compliant and maintain their performance under high-strain deformation. Their stress-relief substrates have a unique structure and utilize pillar arrays to reduce the stress on the active areas of devices when strain is applied.
Traditional intrinsically stretchable OLEDs have commercial limitations due to their low efficiency in the electrical conductivity of the electrodes. In addition, previous geometrically stretchable OLEDs laminated to the elastic substrates with thin film devices lead to different pixel emissions of the devices from different peak sizes of the buckles.
To solve these problems, a research team led by Professor Kyung Cheol Choi designed a stretchable substrate system with surface relief island structures that relieve the stress at the locations of bridges in the devices. Their stretchable OLED devices contained an elastic substrate structure comprising bonded elastic pillars and bridges. A patterned upper substrate with bridges makes the rigid substrate stretchable, while the pillars decentralize the stress on the device.
Although various applications using micropillar arrays have been reported, it has not yet been reported how elastic pillar arrays can affect substrates by relieving the stress applied to those substrates upon stretching. Compared to results using similar layouts with conventional free-standing, flat substrates or island structures, their results with elastic pillar arrays show relatively low stress levels at both the bridges and plates when stretching the devices. They achieved stretchable RGB (red, green, blue) OLEDs and had no difficulties with material selection as practical processes were conducted with stress-relief substrates.
Their stretchable OLEDs were mechanically stable and have two-dimensional stretchability, which is superior to only one-direction stretchable electronics, opening the way for practical applications like wearable electronics and health monitoring systems.
Professor Choi said, “Our substrate design will impart flexibility into electronics technology development including semiconductor and circuit technologies. We look forward this new stretchable OLED lowering the barrier for entering the stretchable display market.”
This research was published in Nano Letters titled Two-Dimensionally Stretchable Organic Light-Emitting Diode with Elastic Pillar Arrays for Stress Relief. (https://dx.doi.org/10.1021/acs.nanolett.9b03657). This work was supported by the Engineering Research Center of Excellence Program supported by the National Research Foundation of Korea.
-Profile
Professor Kyung Cheol Choi
kyungcc@kaist.ac.kr
http://adnc.kaist.ac.kr/
School of Electrical Engineering
KAIST
2020.02.27 View 13328