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KAIST Develops AI Technology to Detect Early Warning Signs of Cerebrovascular Disease at Home
Cerebrovascular disease can lead to serious aftereffects if treatment is delayed, but it is difficult to detect before symptoms appear. KAIST researchers have developed an AI technology that analyzes real-life daily activity and environmental data from older adults to identify digital behavioral markers of cerebrovascular disease risk based on subtle changes at home.
KAIST (President Choongsik Bae) announced on the 12th of July that a research team led by Professor Lisa Lim from the Department of Civil and Environmental Engineering, in collaboration with Professor Jo Woon Chong from the School of Electronic and Electrical Engineering at Sungkyunkwan University (President Ji-Beom Yoo) and Professor Kyung-Hee Cho from the Department of Neurology at Korea University Anam Hospital (President Dongwon Kim), has developed an AI framework that uses long-term lifelog data collected in the homes of older adults to identify the prodromal phase of cerebrovascular disease and assess imminent diagnostic risk.
The study was based on lifelog data from 1,224 older adults collected by LivOn Care Co., Ltd. in real residential environments. The research team analyzed a total of 13,362 two-week lifelog samples, demonstrating the possibility of detecting early warning signs through subtle changes in daily life, rather than relying only on the conventional approach of treating the disease after it has already occurred.
The research team developed AI technology that identifies cerebrovascular disease risk stages by analyzing daily activity, sleep, circadian rhythm, and indoor environmental information, together with age and chronic disease data. This shows that changes in everyday living patterns, which are difficult to capture through hospital examinations alone, can serve as important clues for detecting early risk signals of cerebrovascular disease.
The team also succeeded in assessing whether a cerebrovascular disease diagnosis was approaching by analyzing changes in lifestyle patterns over time. When lifelog data from within four weeks before diagnosis were classified as the “imminent diagnostic risk period” and data from 12 weeks before diagnosis were classified as the “non-imminent period,” the AI distinguished between the two periods with a high accuracy of 96.53%. This result suggests that even before a hospital visit, small changes in daily life may help identify whether the risk of cerebrovascular disease has increased.
Another key feature of this study is that the AI does not simply determine whether a risk exist, but also applies explainable AI to identify the lifestyle patterns and environmental factors behind its judgment.
The analysis showed that older adults in the prodromal phase of cerebrovascular disease tended to show frequent continuous activity between 10 p.m. and 2 a.m., a time when the body would normally be preparing for sleep. In other words, irregular daily rhythms, such as delayed sleep onset and a reduced distinction between day and night activity, were closely associated with prodromal signals of cerebrovascular disease.
The researchers also found that as the time of diagnosis approached, the frequency of continuous activity during the evening period from 6 p.m. to 10 p.m. noticeably decreased, while inactive time increased. Low indoor humidity, indicating a dry indoor environment, also emerged as an important factor in identifying an imminent diagnostic risk.
The research team expects this technology to be used as a digital healthcare tool that can objectively monitor the health status of older adults who may have difficulty clearly describing their own condition, while providing useful early warning indicators to medical professionals and caregivers.
However, the team explained that this study does not predict the exact onset of cerebrovascular disease or replace clinical diagnosis. Rather, it is a supportive technology intended to aid prevention and early medical consultation, and prospective validation in larger patient groups will be necessary before actual clinical application.
Professor Lisa Lim said, “The key point of this study is not that AI should replace a hospital diagnosis, but that it can first detect risk signals in small lifestyle changes at home and help connect patients to medical care at the right time,” adding, “We expect this technology to contribute to a shift from a healthcare system that treats disease after it occurs to one that supports prevention and early intervention.”
This study, with KAIST Dr. Jeongyeop Baek as the first author, was published on June 2 in npj Digital Medicine, a leading international journal in digital healthcare published by Nature Portfolio, with an impact factor of 15.1 and ranked in the top 0.3% of JCR journals.
※ Paper title: AI home monitoring for behavioral markers of cerebrovascular disease
DOI: https://doi.org/10.1038/s41746-026-02836-7
This work was also supported by the National Research Foundation (NRF) grant funded by the Korea government (Ministry of Science and ICT) (RS-2025-16068234).
2026.07.13 View 265 -
KAIST: Dementia-Causing Substance Turns On a Therapeutic “Switch”
A substance that worsens dementia has become a “switch” that initiates treatment. KAIST researchers have developed a new therapeutic approach that uses hydrogen peroxide (H₂O₂), a reactive oxygen species that damages cells and increases in the brains of patients with Alzheimer’s disease, to activate a drug selectively in diseased brain tissue. The team also confirmed improvements in cognitive function through animal experiments, presenting a new possibility for next-generation dementia treatment.
KAIST announced on the 2nd that a research team led by Professor Mi Hee Lim of the Department of Chemistry, in collaboration with Professor Mingeun Kim of Chonnam National University, Dr. Chul-Ho Lee and Dr. Kyoung-Shim Kim of the Korea Research Institute of Bioscience and Biotechnology, and Dr. Young-Ho Lee of the Korea Basic Science Institute, has developed a prodrug that is activated selectively in the diseased brain in Alzheimer’s disease and confirmed its therapeutic effects through animal experiments.
A prodrug is a drug that initially has minimal therapeutic effect but is converted into an active therapeutic agent only under specific conditions inside the body. In this study, the prodrug was designed to be activated only when it encounters hydrogen peroxide, which increases in the brains of patients with Alzheimer’s disease, allowing it to function as a “smart therapeutic agent” that selectively acts in diseased brain tissue.
In the brains of Alzheimer’s disease patients, hydrogen peroxide, which damages cells, is elevated above normal levels. Until now, it has generally been regarded only as a harmful substance that should be removed. However, the research team devised a method to use it instead as a signal that activates a drug.
The prodrugs developed by the research team, BE-1 and BE-2, are designed to remain minimally reactive in a healthy brain. However, when they encounter hydrogen peroxide in a brain affected by dementia, they are converted into active therapeutic compounds, AP-1 and AP-2. Through this process, they reduce reactive oxygen species, including hydrogen peroxide, while also preventing amyloid beta (Aβ) peptides — peptides known as a major cause of dementia that accumulate in the brain and damage nerve cells — from aggregating into highly toxic clumps.
Using advanced analytical techniques, the research team confirmed that the activated drug alters the morphology of amyloid beta aggregates and suppresses their growth into large aggregates.
These effects were also confirmed in Alzheimer’s disease mouse models. The drug crossed the blood-brain barrier (BBB), a protective barrier that controls whether substances in the blood can enter the brain, and was converted into the therapeutic compound inside the diseased brain. In mice that received long-term drug administration, oxidative stress in the hippocampus, which is responsible for memory, was reduced, and amyloid beta accumulation in the brain also decreased. In behavioral experiments assessing the ability to recognize new objects and navigate mazes, cognitive function was also found to improve.
This study is significant in that the drug was designed to operate only where needed by using the environment of the diseased brain itself. This approach presents a new strategy for dementia treatment that can enhance therapeutic efficacy while reducing side effects, and it is expected to be applicable to the treatment of other neurodegenerative diseases, such as Parkinson’s disease.
Professor Mi Hee Lim of KAIST’s Department of Chemistry said, “This study is meaningful in that hydrogen peroxide, which had previously been regarded only as something to be eliminated, was used as a signal to activate a drug. We expect this strategy, which activates drugs in diseased tissue, to become a new platform for treating complex diseases such as Alzheimer’s disease more safely and effectively.”
This study was co-first-authored by Jimin Lee and Eunseo Hong, Ph.D. candidates in KAIST’s Department of Chemistry, and was published online on May 31, 2026, in the international journal Small (Impact Factor: 12.1, top 10% in the field of chemistry).
※ Paper title: A Prodrug Approach for Activity-Based Chemical Modulation toward Multiple Pathological Targets in Alzheimer’s Disease
DOI: 10.1002/smll.74013
This research was supported by the National Research Foundation of Korea’s Leader Researcher Program, Global Leading Research Center Program, Sejong Science Fellowship, Graduate Student Research Encouragement Program, and institutional programs of KRIBB and KBSI.
2026.07.03 View 657 -
Simultaneous Decoding of Genetic Maps Inside Cells... A Game Changer for Understanding Complex Human Diseases
< (Clockwise from top left) Professor Inkyung Jung (KAIST), Dr. Dongchan Yang (KAIST), Dr. Kyukwang Kim (KAIST), Dr. Yueyuan Xu (Duke University), Dr. Xiaolin Wei (Duke University), Professor Yarui Diao (Duke University) >
The origin of many diseases begins at the cellular level and involves multiple molecular interactions. However, previous methods have struggled to accurately observe changes in individual cells. Analyzing average values across thousands of cells made it challenging to detect the early signals of disease.
Our university's research team has pioneered groundbreaking technology that decodes the genetic blueprint within a cell in 3D, akin to zooming in on Earth using Google Earth. This innovation is poised to transform research into complex diseases such as cancer, dementia, and Parkinson's disease.
KAIST announced on March 4th that Professor Inkyung Jung's research team from the Department of Biological Sciences, in collaboration with Professor Yarui Diao's team at Duke University, has developed scHiCAR (single-cell Hi-C with assay for transposase-accessible chromatin and RNA sequencing). This is the world’s first ultra-high throughput & precise molecular map decoding technology that simultaneously analyzes gene expression (transcriptome), the epigenome, and the 3D genome structure within a single cell.
The key to determining a cell's state lies in how its genes operate. Genes are not simply switches that turn on and off. The destiny of a cell is determined by which genes are actually active (transcriptome), why they are active (epigenome), and within what spatial structure they operate (3D genome structure). Existing technologies required obtaining this information from different cells separately and then matching them afterward, which could lead to the distortion or omission of subtle changes.
The research team introduced ‘Trimodal Multi-omics’ technology, an integrated precision analysis method that concurrently examines these three types of genetic information within a single cell. By incorporating Artificial Intelligence (AI) analysis, they significantly enhanced accuracy and reproducibility, culminating in a unified platform that reads internal cellular genetic information akin to a ‘single 3D map.’
<Ultra-precision Single-cell Molecular Map>
Notably, the team succeeded in lowering the analysis cost to approximately $0.04 (approx. 50 KRW) per cell. Using this, they constructed a high-resolution molecular map of 1.6 million cells in mouse brain tissue. This means it is now possible to precisely identify when, where, and within what structure disease genes are turned on or off at the cellular level.
The research team applied this technology to brain tissue and the muscle regeneration process, revealing distinct gene operation principles across 22 major cell types. Notably, they successfully tracked in real-time how the 3D structure of genes dynamically changes to influence cell fate during muscle stem cell regeneration. This advancement is expected to lay a crucial foundation for developing treatment strategies for aging and incurable diseases.
<Research Result Image (AI-generated)>
Professor Inkyung Jung remarked, ‘This research transcends mere observation of cells; it opens the door to precisely reading and controlling the genomic blueprints within them. It represents a significant turning point in elucidating the developmental mechanisms of complex diseases like Parkinson's and cancer, as well as identifying target points for patient-specific new drugs.’
The study was published on February 19th in the international academic journal Nature Biotechnology (IF=46.9).
Paper Title: Trimodal single-cell profiling of transcriptome, epigenome and 3D genome in complex tissues with scHiCAR
DOI: 10.1038/s41587-026-03013-7
Meanwhile, this research was conducted with support from the Suh Kyungbae Foundation, the Samsung Science and Technology Foundation, and the Basic Research Program and Bio-Medical Technology Development Program of the National Research Foundation of Korea (Ministry of Science and ICT).
2026.03.06 View 1549 -
Discovery of a Switch to Halt Adipocyte Generation
< (From left) Dr. Ju-Gyeong Kang, Ph.D candidate TaeJun Seol, Professor Dae-Sik Lim >
Metabolic diseases such as obesity, fatty liver, and insulin resistance are rapidly increasing worldwide, but fundamental methods to regulate the process of fat formation remain limited. In particular, once adipocytes (fat cells) are formed, they are difficult to reduce, making treatment challenging. Amidst this, a research team from our university has discovered the existence of a ‘switch’ that prevents fat formation. This discovery elucidates how an ‘epigenetic switch’—which regulates gene activity without altering the DNA sequence itself—functions during the process of adipogenesis, presenting new possibilities for the precise control of obesity and metabolic diseases in the future.
The research team, led by Professor Dae-Sik Lim and Professor Ju-Gyeong Kang from KAIST’s Department of Biological Sciences, announced on January 25th that they have identified ‘YAP/TAZ,’ key regulators of the Hippo signaling pathway*, as playing the role of an ‘epigenetic differentiation inhibition switch’ during the process of adipocyte differentiation**. The team proposed a new mechanism in which YAP/TAZ extensively inhibits the activation of genes responsible for adipocyte formation through its downstream target, ‘VGLL3.’ *Hippo signaling pathway: A cellular control system that regulates when cells grow, stop dividing, and differentiate. **Adipocyte differentiation: The process by which preadipocytes (or stem cells) transform into mature adipocytes.
Cell differentiation is not a simple matter of a single gene turning on or off; it is a complex, organic process involving multiple genes and DNA regulatory regions. The research team tracked the entire process of preadipocytes* differentiating into adipocytes using Next-Generation Sequencing (NGS), which allows for the simultaneous analysis of gene expression changes and epigenetic modifications. *Preadipocyte: A developing intermediate-stage cell whose direction as to which cell it will become has already been determined.
As a result, they confirmed that under conditions where YAP/TAZ is activated, the genetic program that establishes adipocyte identity fails to operate, and the overall adipocyte differentiation network—centered around PPARγ*—is suppressed. *PPARγ: The ‘metabolic master switch’ regulator that controls energy storage and utilization in the body.
Specifically, through single-cell analysis of adipose tissue, the research team identified VGLL3 as a novel target gene of YAP/TAZ. While it was previously known that YAP/TAZ directly binds to and inhibits PPARγ, this study revealed that VGLL3 indirectly controls the entire adipocyte differentiation program by suppressing ‘enhancers,’ which are the DNA regulatory regions of adipocyte genes. This signifies that the Hippo signaling pathway plays a crucial role in regulating the core timing that determines when and how robustly fat cells are created.
Dysfunction of adipose tissue is deeply linked to various metabolic diseases such as obesity, insulin resistance, and fatty liver. The research team expects that further studies on how the YAP/TAZ–VGLL3–PPARγ axis regulatory principle involves adipocyte formation and functional abnormalities will provide new clues for regulating or treating metabolic diseases.
< Schematic Diagram of Adipocyte Gene Regulation >
Professor Dae-Sik Lim stated, “This study is the first to establish that adipocyte differentiation is precisely controlled at the epigenetic level, beyond simple gene regulation. It has laid an important foundation for a more sophisticated understanding of the mechanisms behind adipocyte identity changes and, in the long term, for developing personalized treatment strategies for patients with metabolic diseases.”
This research, with Ph.D. student TaeJun Seol and Dr. Ju-Gyeong Kang as co-first authors, was published on January 14th in the world-renowned international academic journal, Science Advances. ※ Paper Title: YAP/TAZ-VGLL3 governs adipocyte fate via epigenetic reprogramming of PPARγ and its target enhancers, DOI: 10.1126/sciadv.aea7235
Meanwhile, this research was conducted with support from the Leader Researcher Support Program and the Overseas Excellent Scientist Recruitment Program of the National Research Foundation of Korea, funded by the Ministry of Science and ICT.
2026.01.26 View 2335 -
Breakthrough in Intractable Intestinal Disease Treatment Using Xenogeneic-Free Intestinal Stem Cells
< (From left) Professor Sung Gap Im (KAIST), Dr. Seonghyeon Park (KAIST), M.S candidate Sang Yu Sun (KAIST), Dr. Mi-Young Son (KRIBB), (Top right) Dr. Tae Geol Lee (KRISS), Dr. Jin Gyeong Son (KRISS) >
Intestinal Stem Cells (ISCs) derived from a patient's own cells have garnered significant attention as a new alternative for treating intractable intestinal diseases due to their low risk of rejection. However, clinical application has been limited by safety and regulatory issues arising from conventional culture methods that rely on animal-derived components (xenogeneic components). A KAIST research team has developed an advanced culture technology that stably grows ISCs without animal components while simultaneously enhancing their migration to damaged tissues and regenerative capabilities.
KAIST announced on December 23rd that a joint research team—led by Professor Sung Gap Im from the Department of Chemical and Biomolecular Engineering, Dr. Tae Geol Lee from the Nano-Bio Measurement Group at the Korea Research Institute of Standards and Science and Dr. Mi-Young Son from the Stem Cell Convergence Research Center at the Korea Research Institute of Bioscience and Biotechnology has developed a polymer-based culture platform that dramatically improves the migration and regeneration of ISCs in a xenogeneic-free environment.
To overcome obstacles in the clinical application of stem cell therapies—such as the risk of virus transmission to patients when using substances derived from mouse fibroblasts or Matrigel—the joint research team developed "PLUS" (Polymer-coated Ultra-stable Surface). This polymer-based culture surface technology functions effectively without any animal-derived materials.
< Figure 1. Precise control of polymer coating and surface modification via initiated Chemical Vapor Deposition (iCVD) process >
PLUS is a synthetic polymer surface coated via a vapor deposition method. By precisely controlling surface energy and chemical composition, it significantly enhances the adhesion and mass-culture efficiency of ISCs. Notably, it maintains identical culture performance even after being stored at room temperature for three years, securing industrial scalability and storage convenience for stem cell therapeutics.
Through proteomics analysis*, the research team identified that the expression of proteins related to cytoskeletal reorganization significantly increased in ISCs cultured on the PLUS environment.
Proteomics Analysis: A method used to simultaneously analyze the types and quantitative changes of all proteins present within a cell or tissue.
Specifically, the team confirmed that increased expression of cytoskeleton-binding and actin-binding proteins leads to a stable restructuring of the internal cellular architecture. This provides the power source for stem cells to move faster and more actively across the substrate.
< Figure 2. Elucidation of the mechanism for enhanced ISC migration through precision proteomics analysis >
Real-time observations using holotomography microscopy revealed that ISCs cultured on PLUS exhibited a migration speed approximately twice as fast as those on conventional surfaces. Furthermore, in a damaged tissue model, the cells demonstrated outstanding regenerative performance, repairing more than half of the damage within a single week. This proves that PLUS activates the cytoskeletal activity of stem cells, thereby boosting their practical tissue regeneration capabilities.
The newly developed PLUS culture platform is evaluated as a technology that will significantly enhance the safety, mass production, and clinical feasibility of ISCs derived from human pluripotent stem cells (hPSCs). By elucidating the mechanism that simultaneously strengthens the survival, migration, and regeneration of stem cells in a xenogeneic-free environment, the team has established a foundation to fundamentally resolve safety, regulatory, and productivity issues in stem cell therapy.
Professor Sung Gap Im of KAIST stated, "This research provides a synthetic culture platform that eliminates the dependence on xenogeneic components—which has hindered the clinical application of stem cell therapies—while maximizing the migration and regenerative capacity of stem cells. It will serve as a catalyst for a paradigm shift in the field of regenerative medicine."
Dr. Seonghyeon Park (KAIST), Sang Yu Sun (KAIST), and Dr. Jin Gyeong Son (KRISS) participated as first authors. The research findings were published online on November 26th in Advanced Materials, the leading academic journal in materials science.
Paper Title: Tailored Xenogeneic-Free Polymer Surface Promotes Dynamic Migration of Intestinal Stem Cells
DOI: 10.1002/adma.202513371
This research was conducted with support from the Ministry of Science and ICT, the Ministry of SMEs and Startups, the National Research Foundation of Korea, the National Council of Science and Technology Research, KRISS, KRIBB, and the National NanoFab Center.
2025.12.23 View 2382 -
KAIST Professors Participate in Mastering Immunity 2025 Singapore Summit
<2025 Global Infectious Diseases Summit>
KAIST is proud to announce the participation of Professors Eui-Cheol Shin and Jeong Seok Lee in the Mastering Immunity 2025: Global Infectious Diseases Summit, held on 1–2 September 2025 in Singapore. This international symposium brought together leading experts in immunology to discuss the latest advancements in infectious disease research, vaccine development, and immune response characterization.
At the summit, Professor Eui-Cheol Shin contributed as a speaker, sharing insights from his groundbreaking research in immunology, while Professor Jeong Seok Lee also presented on his latest work in the field. Professor Eui-Cheol Shin joined a panel discussion alongside other distinguished global experts, highlighting the importance of collaboration in addressing pressing infectious disease challenges.
The summit was organized by ProImmune, an international life-science company specializing in innovative immunology solutions. Through cutting-edge technologies, including Ankyron® target-binding reagents, Pro5® MHC Class I Pentamers, ProT2® MHC Class II Tetramers as well as immunology-based assays such as REVEAL® MHC Binding Assays and ProPresent® Antigen Presentation Assays are accelerating this vital research. ProImmune supports researchers worldwide in understanding immune responses and accelerating the development of vaccines and immunotherapies.
<Presentation at the Summit>
KAIST celebrates the contributions of Professors Shin and Lee in representing Korean science on the global stage and advancing the understanding of infectious diseases.
For more information about the Mastering Immunity 2025 summit and to view the recorded talks, visit: https://www.proimmune.com/conference-videos
2025.09.13 View 2520 -
KAIST Enables On-Site Disease Diagnosis in Just 3 Minutes... Nanozyme Reaction Selectivity Improved 38-Fold
<(From Left) Professor Jinwoo Lee, Ph.D candidate Seonhye Park and Ph.D candidate Daeeun Choi from Chemical & Biomolecular Engineering>
To enable early diagnosis of acute illnesses and effective management of chronic conditions, point-of-care testing (POCT) technology—diagnostics conducted near the patient—is drawing global attention. The key to POCT lies in enzymes that recognize and react precisely with specific substances. However, traditional natural enzymes are expensive and unstable, and nanozymes (enzyme-mimicking catalysts) have suffered from low reaction selectivity. Now, a Korean research team has developed a high-sensitivity sensor platform that achieves 38 times higher selectivity than existing nanozymes and allows disease diagnostics visible to the naked eye within just 3 minutes.
On the 28th, KAIST (President Kwang Hyung Lee) announced that Professor Jinwoo Lee’s research team from the Department of Chemical & Biomolecular Engineering, in collaboration with teams led by Professor Jeong Woo Han at Seoul National University and Professor Moon Il Kim at Gachon University, has developed a new single-atom catalyst that selectively performs only peroxidase-like reactions while maintaining high reaction efficiency.
Using bodily fluids such as blood, urine, or saliva, this diagnostic platform enables test results to be read within minutes even outside hospital settings—greatly improving medical accessibility and ensuring timely treatment. The key lies in the visual detection of biomarkers (disease indicators) through color changes triggered by enzyme reactions. However, natural enzymes are expensive and easily degraded in diagnostic environments, limiting their storage and distribution.
To address this, inorganic nanozyme materials have been developed as substitutes. Yet, they typically lack selectivity—when hydrogen peroxide is used as a substrate, the same catalyst triggers both peroxidase-like reactions (which cause color change) and catalase-like reactions (which remove the substrate), reducing diagnostic signal accuracy.
To control catalyst selectivity at the atomic level, the researchers used an innovative structural design: attaching chlorine (Cl) ligands in a three-dimensional configuration to the central ruthenium (Ru) atom to fine-tune its chemical properties. This enabled them to isolate only the desired diagnostic signal.
<Figure1. The catalyst in this study (ruthenium single-atom catalyst) exhibits peroxidase-like activity with selectivity akin to natural enzymes through three-dimensional directional ligand coordination. Due to the absence of competing catalase activity, selective peroxidase-like reactions proceed under biomimetic conditions. In contrast, conventional single-atom catalysts with active sites arranged on planar surfaces exhibit dual functionality depending on pH. Under neutral conditions, their catalase activity leads to hydrogen peroxide depletion, hindering accurate detection. The catalyst in this study eliminates such interference, enabling direct detection of biomarkers through coupled reactions with oxidases without the need for cumbersome steps like buffer replacement. The ability to simultaneously detect multiple target substances under biomimetic conditions demonstrates the practicality of ruthenium single-atom catalysts for on-site diagnostics>
Experimental results showed that the new catalyst achieved over 38-fold improvement in selectivity compared to existing nanozymes, with significantly increased sensitivity and speed in detecting hydrogen peroxide. Even in near-physiological conditions (pH 6.0), the catalyst maintained its performance, proving its applicability in real-world diagnostics.
By incorporating the catalyst and oxidase into a paper-based sensor, the team created a system that could simultaneously detect four key biomarkers related to health: glucose, lactate, cholesterol, and choline—all with a simple color change.
This platform is broadly applicable across various disease diagnostics and can deliver results within 3 minutes without complex instruments or pH adjustments. The findings show that diagnostic performance can be dramatically improved without changing the platform itself, but rather by engineering the catalyst structure.
<Figure 2.(a) Schematic diagram of the paper sensor (Zone 1: glucose oxidase immobilized; Zone 2: lactate oxidase immobilized; Zone 3: choline oxidase immobilized; Zone 4: cholesterol oxidase immobilized; Zone 5: no oxidase enzyme). (b) Single biomarker (single disease indicator) detection using the ruthenium single‑atom catalyst–based paper sensor.(c) Multiple biomarker (multiple disease indicator) detection using the ruthenium single‑atom catalyst–based paper sensor>
Professor Jinwoo Lee of KAIST commented, “This study is significant in that it simultaneously achieves enzyme-level selectivity and reactivity by structurally designing single-atom catalysts.” He added that “the structure–function-based catalyst design strategy can be extended to the development of various metal-based catalysts and other reaction domains where selectivity is critical.”
Seonhye Park and Daeeun Choi, both Ph.D. candidates at KAIST, are co-first authors. The research was published on July 6, 2025, in the prestigious journal Advanced Materials
-Title: Breaking the Selectivity Barrier of Single-Atom Nanozymes Through Out-of-Plane Ligand Coordinatio
- Authors: Seonhye Park (KAIST, co–first author), Daeeun Choi (KAIST, co–first author), Kyu In Shim (SNU, co–first author), Phuong Thy Nguyen (Gachon Univ., co–first author), Seongbeen Kim (KAIST), Seung Yeop Yi (KAIST), Moon Il Kim (Gachon Univ., corresponding author), Jeong Woo Han (SNU, corresponding author), Jinwoo Lee (KAIST, corresponding author
-DOI: https://doi.org/10.1002/adma.202506480
This research was supported by the Ministry of Science and ICT and the National Research Foundation of Korea (NRF).
2025.07.29 View 4393 -
KAIST Discovers Protein Switch that Turns Anti-Viral Immune Response On and Off
Even after the COVID-19 pandemic, various new infectious diseases continue to emerge, posing ongoing viral threats that demand robust and sustained immune defenses. However, excessive immune reactions can also harm body tissues, causing significant health issues. KAIST and an international research team have discovered a critical protein that acts as a 'switch' regulating immune responses to viruses. This breakthrough is expected to lay the groundwork for future infectious disease responses and autoimmune disease treatment strategies.
KAIST (President Kwang-Hyung Lee) announced on May 14 that a joint research team led by Professor Yoosik Kim from the Department of Chemical and Biomolecular Engineering at KAIST and Professor Seunghee Cha from University of Florida has discovered the mechanism by which double-stranded RNA derived from mitochondria amplifies immune responses. They identified the protein SLIRP as an 'immune switch' that regulates this process, playing a crucial role in both viral infections and autoimmune diseases.
< (From left) Master's candidate Yewon Yang, Professor Yoosik Kim and Ph.D. candidate Doyeong Ku of the Department of Chemical and Biomolecular Engineering >
Autoimmune diseases arise when the immune system fails to differentiate between external pathogens and the body's own molecules, leading to self-directed attacks. Despite extensive research, the precise causes of excessive inflammatory conditions like Sjögren’s syndrome and systemic lupus erythematosus remain unclear, and effective treatments are still limited.
To uncover the molecular mechanisms driving immune hyperactivation and to identify potential regulatory factors, the research team led by Professor Yoosik Kim focused on mitochondrial double-stranded RNA (mt-dsRNA), a genetic immunogenic material produced within cellular organelles. Since mt-dsRNA structurally resembles viral RNA, it can mistakenly trigger immune responses even in the absence of an actual viral infection.
The team discovered that SLIRP, a key regulator of mt-dsRNA, amplifies immune responses by stabilizing the RNA. They confirmed that SLIRP expression increases in experimental models simulating the tissues of autoimmune disease patients and viral infections. Conversely, suppressing SLIRP significantly reduced the immune response, underscoring its role as a critical factor in immune amplification.
This study also demonstrated the dual function of SLIRP in different contexts. In cells infected with human beta coronavirus OC43 and encephalomyocarditis virus (EMCV), SLIRP suppression led to reduced antiviral responses and increased viral replication. Meanwhile, in the blood and salivary gland cells of Sjögren’s syndrome patients, where both SLIRP and mt-dsRNA levels were elevated, suppressing SLIRP alleviated the abnormal immune response.
These findings highlight SLIRP as a key molecular switch that regulates immune responses in both infections and autoimmune diseases.
< Figure 1. Schematic diagram of antiviral signal amplification by SLIRP: SLIRP-based mt-dsRNA induction, cytoplasmic accumulation, and strong interferon response induction by positive feedback of immune response activation. Confirmation of the immune regulatory function of SLIRP in defense against autoimmune diseases Sjögren's syndrome, coronavirus, and encephalomyocarditis virus infection. >
Professor Yoosik Kim remarked, "Through this study, we have identified SLIRP as a crucial protein that drives immune amplification via mt-dsRNAs. Given its dual role in autoimmune diseases and viral infections, SLIRP presents a promising target for immune regulation therapies across various inflammatory disease contexts."
The study, with Ph.D. student Do-Young Ku (first author) and M.S. student Ye-Won Yang (second author) from the Department of Chemical and Biomolecular Engineering at KAIST as primary contributors, was published online in the journal Cell Reports on April 19, 2025.
※ Paper title: SLIRP amplifies antiviral signaling via positive feedback regulation and contributes to autoimmune diseases※ Main authors: Do-Young Ku (KAIST, first author), Ye-Won Yang (KAIST, second author), Seunghee Cha (University of Florida, corresponding author), Yoosik Kim (KAIST, corresponding author)
This study was supported by the Ministry of Health and Welfare's Public Health Technology Research Program and the National Institutes of Health (NIH) through Research Project (R01) funding.
2025.05.14 View 8973 -
Editing Parkinson's Disease – KAIST Makes World's First Discovery of an Inflammatory RNA Editing Enzyme through Co-work with UCL Researchers
< Professor Minee Choi of the Department of Brain and Cognitive Sciences (top left). Professor Sonia Gandhi (top right) and Professor Klenerman of the University College London (bottom right) >
Parkinson's disease (PD) is a neurodegenerative disorder in which the α-synuclein protein abnormally aggregates within brain cells, causing neuronal damage. Through international collaboration, researchers at KAIST have revealed that RNA editing plays a crucial role in regulating neuroinflammation, a key pathology of Parkinson's disease.
KAIST (represented by President Kwang-Hyung Lee) announced on the 27th of April that a research team led by Professor Minee L. Choi from the Department of Brain and Cognitive Sciences, in collaboration with University College London (UCL) and the Francis Crick Institute, discovered that the RNA editing enzyme ADAR1 plays an important role in controlling immune responses in astrocytes, glial cells that trigger protective reactions in the brain, and demonstrated that this mechanism is critically involved in the progression of Parkinson’s disease.
Professor Choi's research team created a co-culture model composed of astrocytes and neurons derived from stem cells originating from Parkinson's disease patients, in order to study the inflammatory responses of brain immune cells. They then treated the model with α-synuclein aggregates, which are known to cause Parkinson’s disease, and analyzed how the immune cells' inflammatory responses changed.
< Figure 1. Schematic diagram of the inflammatory RNA editing model in Parkinson's disease >
As a result, it was found that early pathological forms of α-synuclein, known as oligomers, activated the Toll-like receptor pathway, which acts as a danger sensor in astrocytes, as well as the interferon response pathway, an immune signaling network that combats viruses and pathogens. During this process, the RNA editing enzyme ADAR1 was expressed and transformed into an isoform with an altered protein structure and function.
Notably, the RNA editing activity of ADAR1, which normally functions to regulate immune responses during viral infections by converting adenosine (A) to inosine (I) through a process known as A-to-I RNA editing, was found to be abnormally focused on genes that cause inflammation rather than operating under normal conditions. This phenomenon was observed not only in the patient-derived neuron models but also in postmortem brain tissues from actual Parkinson’s disease patients.
< Figure 2. Experimental design and inflammatory response induction in astrocytes following treatment with α-synuclein oligomers (abnormally folded protein fragments) >
This directly proves that the dysregulation of RNA editing induces chronic inflammatory responses in astrocytes, ultimately leading to neuronal toxicity and pathological progression.
This study is significant in that it newly identified the regulation of RNA editing within astrocytes as a key mechanism behind neuroinflammatory responses. In particular, it suggests that ADAR1 could serve as a novel genetic target for the treatment of Parkinson’s disease.
It is also noteworthy that the study reflected actual pathological characteristics of patients by utilizing patient-specific induced pluripotent stem cell-based precision models for brain diseases.
Professor Minee L. Choi stated, “This study demonstrates that the regulator of inflammation caused by protein aggregation operates at the new layer of RNA editing, offering a completely different therapeutic strategy from existing approaches to Parkinson's disease treatment." She further emphasized, “RNA editing technology could become an important turning point in the development of therapeutics for neuroinflammation.”
< Figure 3. When treated with α-synuclein oligomers, the causative agent of Parkinson's disease, A-to-I RNA editing is induced to change genetic information by ADAR in patient-derived stem cell-differentiated glial cells, confirming that α-synuclein is likely to be associated with the progression of Parkinson's disease through RNA editing >
This study was published in Science Advances on April 11, with Professor Choi listed as a co-first author.
Paper Title: Astrocytic RNA editing regulates the host immune response to alpha-synuclein, Science Advances Vol.11, Issue 15. (DOI:10.1126/sciadv.adp8504)
Lead Authors: Karishma D’Sa (UCL, Co-First Author), Minee L. Choi (KAIST, Co-First Author), Mina Ryten (UCL, Corresponding Author), Sonia Gandhi (Francis Crick Institute, University of Cambridge, Corresponding Author)
This research was supported by the Brain Research Program and the Excellent Young Researcher Program of the National Research Foundation of Korea, as well as KAIST’s Daekyo Cognitive Enhancement Program.
2025.05.02 View 10645 -
KAIST Develops Retinal Therapy to Restore Lost Vision
Vision is one of the most crucial human senses, yet over 300 million people worldwide are at risk of vision loss due to various retinal diseases. While recent advancements in retinal disease treatments have successfully slowed disease progression, no effective therapy has been developed to restore already lost vision—until now. KAIST researchers have successfully developed a novel drug to restore vision.
< Photo 1. (From left) Ph.D. candidate Museong Kim, Professor Jin Woo Kim, and Dr. Eun Jung Lee of KAIST Department of Biological Sciences >
KAIST (represented by President Kwang Hyung Lee) announced on the 30th of March that a research team led by Professor Jin Woo Kim from the Department of Biological Sciences has developed a treatment method that restores vision through retinal nerve regeneration.
The research team successfully induced retinal regeneration and vision recovery in a disease-model mouse by administering a compound that blocks the PROX1 (prospero homeobox 1) protein, which suppresses retinal regeneration. Furthermore, the effect lasted for more than six months.
This study marks the first successful induction of long-term neural regeneration in mammalian retinas, offering new hope to patients with degenerative retinal diseases who previously had no treatment options.
As the global population continues to age, the number of retinal disease patients is steadily increasing. However, no treatments exist to restore damaged retinas and vision. The primary reason for this is the mammalian retina's inability to regenerate once damaged.
Studies on cold-blooded animals, such as fish—known for their robust retinal regeneration—have shown that retinal injuries trigger Müller glia cells to dedifferentiate into retinal progenitor cells, which then generate new neurons. However, in mammals, this process is impaired, leading to permanent retinal damage.
< Figure 1. Schematic diagram of the mechanism of retinal regeneration through inhibition of PROX1 migration. PROX1 protein secreted from retinal damaged retinal neurons transfers to Müllerglia and inhibits dedifferentiation into neural progenitor cells and neural regeneration. When PROX1 is captured outside the cells by an antibody against PROX1 and its transfer to Müllerglia is interfered, dedifferentiation of Müllerglia cells and retinal regeneration processes are resumed, restoring visual function. >
Through this study, the research team identified the PROX1 protein as a key inhibitor of Müller glia dedifferentiation in mammals. PROX1 is a protein found in neurons of the retina, hippocampus, and spinal cord, where it suppresses neural stem cell proliferation and promotes differentiation into neurons.
The researchers discovered that PROX1 accumulates in damaged mouse retinal Müller glia, but is absent in the highly regenerative Müller glia of fish. Furthermore, they demonstrated that the PROX1 found in Müller glia is not synthesized internally but rather taken up from surrounding neurons, which fail to degrade and instead secrete the protein.
Based on this finding, the team developed a method to restore Müller glia’s regenerative ability by eliminating extracellular PROX1 before it reaches these cells.
< Figure 2. Retinal regeneration and visual recovery in a retinitis pigmentosa model mouse through Anti-PROX1 gene therapy. After administration of adeno-associated virus expressing PROX1 neutralizing antibodies (AAV2-Anti-PROX1) to the eyes of RP1 retinitis pigmentosa model mice with vision loss, the photoreceptor cell layer of the retina is restored (A) and vision is restored (B). >
This approach involves using an antibody that binds to PROX1, developed by Celliaz Inc., a biotech startup founded by Professor Jin Woo Kim’s research lab. When administered to disease-model mouse retinas, this antibody significantly promoted neural regeneration. Additionally, when delivered, the antibody gene to the retinas of retinitis pigmentosa disease model mice, it enabled sustained retinal regeneration and vision restoration for over six months.
The retinal regeneration-inducing therapy is currently being developed by Celliaz Inc. for application in various degenerative retinal diseases that currently lack effective treatments. The company aims to begin clinical trials by 2028.
This study was co-authored by Dr. Eun Jung Lee of Celliaz Inc. and Museong Kim, a Ph.D. candidate at KAIST, as joint first authors. The findings were published online on March 26 in the international journal Nature Communications. (Paper Title: Restoration of retinal regenerative potential of Müller glia by disrupting intercellular Prox1 transfer | DOI: 10.1038/s41467-025-58290-8)
Dr. Eun Jung Lee stated, "We are about completing the optimization of the PROX1-neutralizing antibody (CLZ001) and move to preclinical studies before administering it to retinal disease patients. Our goal is to provide a solution for patients at risk of blindness who currently lack proper treatment options."
This research was supported by research funds from Korean National Research Foundation (NRF) and the Korea Drug Development Foundation (KDDF).
2025.03.31 View 29357 -
KAIST to Collaborate with AT&C to Take Dominance over Dementia
< Photo 1. (From left) KAIST Dean of the College of Natural Sciences Daesoo Kim, KAIST President Kwang Hyung Lee, AT&C Chairman Ki Tae Lee, AT&C CEO Jong-won Lee >
KAIST (President Kwang Hyung Lee) announced on January 9th that it signed a memorandum of understanding for a comprehensive mutual cooperation with AT&C (CEO Jong-won Lee) at its Seoul Dogok Campus to expand research investment and industry-academia cooperation in preparation for the future cutting-edge digital bio era.
Senile dementia is a rapidly increasing brain disease that affects 10% of the elderly population aged 65 and older, and approximately 38% of those aged 85 and older suffer from dementia. Alzheimer's disease is the most common dementia in the elderly and its prevalence has been increasing rapidly in the population of over 40 years of age. However, an effective treatment is yet to be found.
The Korean government is investing a total of KRW 1.1 trillion in dementia R&D projects from 2020 to 2029, with the goal of reducing the rate of increase of dementia patients by 50%. Since it takes a lot of time and money to develop effective and affordable medicinal dementia treatments, it is urgent to work on the development of digital treatments for dementia that can be applied more quickly.
AT&C, a digital healthcare company, has already received approval from the Ministry of Food and Drug Safety (MFDS) for its device for antidepressant treatment based on transcranial magnetic stimulation (TMS) using magnetic fields and is selling it domestically and internationally. In addition, it has developed the first Alzheimer's dementia treatment device in Korea and received MFDS approval for clinical trials. After passing phase 1 to evaluate safety and phase 2 to test efficacy on some patients, it is currently conducting phase 3 clinical trials to test efficacy on a larger group of patients.
This dementia treatment device is equipped with a system that combines non-invasive electronic stimulations (TMS electromagnetic stimulator) and digital therapeutic prescription (cognitive learning programs) to provide precise, automated treatment by applying AI image analysis and robotics technology.
Through this agreement, KAIST and AT&C have agreed to cooperate with each other in the development of innovative digital treatment equipment for brain diseases. Through research collaboration with KAIST, AT&C will be able to develop technology that can be widely applied to Parkinson's disease, stroke, mild cognitive impairment, sleep disorders, etc., and will develop portable equipment that can improve brain function and prevent dementia at home by utilizing KAIST's wearable technology.
To this end, AT&C plans to establish a digital healthcare research center at KAIST by supporting research personnel and research expenses worth approximately 3 billion won with the goal of developing cutting-edge digital equipment within 3 years.
The digital equipment market is expected to grow at a compounded annual growth rate of 22.1% from 2023 to 2033, reaching a market size of $1.9209 trillion by 2033.
< Photo 2. (From left) Dean of the KAIST College of Natural Sciences Daesoo Kim, Professor Young-joon Lee, Professor Minee Choi of the KAIST Department of Brain and Cognitive Sciences, KAIST President Kwang Hyung Lee, Chairman Ki Tae Lee, CEO Jong-won Lee, and Headquarters Director Ki-yong Na of AT&C >
CEO Jong-won Lee said, “AT&C is playing a leading role in the treatment of Alzheimer’s disease using TMS (transcranial magnetic stimulation) technology. Through this agreement with KAIST, we will do our best to create a new paradigm for brain disease treatment and become a platform company that can lead future medical devices and medical technology.”
Former Samsung Electronics Vice Chairman Ki Tae Lee, a strong supporter of this R&D project, said, “Through this agreement with KAIST, we plan to prepare for a new future by combining the technologies AT&C has developed so far with KAIST’s innovative and differentiated technologies.”
KAIST President Kwang Hyung Lee emphasized, “Through this collaboration, KAIST expects to build a world-class digital therapeutics infrastructure for treating brain diseases and contribute greatly to further strengthening Korea’s competitiveness in the biomedical field.”
The signing ceremony was attended by KAIST President Kwang Hyung Lee, the Dean of KAIST College of Natural Sciences Daesoo Kim, AT&C CEO Lee Jong-won, and the current Chairman of AT&C, Ki Tae Lee, former Vice Chairman of Samsung Electronics.
2025.01.09 View 11832 -
A Korean research team develops a new clinical candidate for fatty liver disease
A team of Korean researchers have succeeded in developing a new drug candidate for the treatment of non-alcoholic fatty liver disease (NAFLD) acting on peripheral tissues. To date, there has not been an optimal treatment for non-alcoholic steatohepatitis (NASH), and this discovery is expected to set the grounds for the development of new drugs that can safely suppress both liver fat accumulation and liver fibrosis at the same time.
A joint research team led by Professor Jin Hee Ahn from Gwangju Institute of Science and Technology (GIST) and Professor Hail Kim from the KAIST Graduate School of Medical Science and Engineering developed a new chemical that can suppress disease-specific protein (HTR2A) through years of basic research. The team also revealed to have verified its efficacy and safety through preclinical tests (animal tests) at JD Bioscience Inc., a start-up company founded by Professor Ahn.
Although NAFLD has a prevalence rate as high as 20-30%, and about 5% of the global adult population suffers from NASH, there are no commercial drugs targeting them to date. NAFLD is a chronic disease that starts from the fatty liver and progresses into steatohepatitis, fibrosis, cirrhosis, and liver cancer. The mortality rate of patients increases with accompanied cardiovascular diseases and liver-related complications, and appropriate treatment in the early stage is hence necessary.
< Figure 1. Strategy and history of 5HT2A antagonists. Library and rational design for the development of compound 11c as a potent 5HT2A antagonist. Previous research efforts were discontinued due to limited oral absorption and safety. A therapeutic candidate to overcome this problem was identified and phase 1 clinical trials are currently in progress. >
The new synthetic chemical developed by the joint GIST-KAIST research is an innovative drug candidate that shows therapeutic effects on NASH based on a dual action mechanism that inhibits the accumulation of fat in the liver and liver fibrosis by suppressing the serotonin receptor protein 5HT2A.
The research team confirmed its therapeutic effects in animal models for NAFLD and NASH, in which hepatic steatosis and liver fibrosis* caused by fat accumulation in the liver were suppressed simultaneously by 50-70%.
*fibrosis: stiffening of parts of the liver, also used as a major indicator to track the prognosis of steatosis
The research team explained that the material was designed with optimal polarity and lipid affinity to minimize its permeability across the blood-brain barrier. It therefore does not affect the brain, and causes little side effects in the central nervous system (CNS) such as depression and suicidal ideations, while demonstrating excellent inhibition on its target protein present in tissues outside brain (IC50* = 14 nM). The team also demonstrated its superior efficacy in improving liver fibrosis when compared to similar drugs in the phase 3 clinical trial.
*IC50 (half maximal inhibitory concentration): the concentration at which a chemical suppresses 50% of a particular biological function
< Figure 2. GM-60106 (11c)'s effect on obesity: When GM-60106 was administered to an obese animal model (mice) for 2 months, body weight, body fat mass, and blood sugar were significantly reduced (a-d). In addition, the steatohepatitis level (NAFLD Activity Score) and the expression of genes of the treated mice involved in adipogenesis along with blood/liver fat decreased (e-h) >
Based on the pharmacological data obtained through preclinical trials, the team evaluated the effects of the drug on 88 healthy adults as part of their phase 1 clinical trial, where the side effects and the safe dosage of a drug are tested against healthy adults. Results showed no serious side effects and a good level of drug safety.
In addition, a preliminary efficacy evaluation on eight adults with steatohepatitis is currently underway.
Professor Jin Hee Ahn said, “The aim of this research is to develop a treatment for NASH with little side effects and guaranteed safety by developing a new target. The developed chemical is currently going through phase 1 of the global clinical trial in Australia through JD Bioscience Inc., a bio venture company for innovative drug development.” he added, “The candidate material the research team is currently developing shows not only a high level of safety and preventative effects by suppressing fat accumulation in the liver, but also a direct therapeutic effect on liver fibrosis. This is a strength that distinguishes our material from other competing drugs.”
< Figure 3. Efficacy of GM-60106 (11c) on liver fibrosis: When GM-60106 was administered to a steatohepatitis model (mice) for 3 months, the expression of genes associated with tissue fibrosis was significantly reduced (b-c). As a result of a detailed analysis of the tissues of the animal model, it was confirmed that the rate of tissue fibrosis was reduced and the expression rate of genes related to tissue fibrosis and inflammation was also significantly reduced (e-h). >
Professor Hail Kim from KAIST said, “Until now, this disease did not have a method of treatment other than weight control, and there has been no attempt to develop a drug that can be used for non-obese patients.” He added, “Through this research, we look forward to the development of various treatment techniques targeting a range of metabolic diseases including NASH that do not affect the weight of the patient.”
This study, conducted together by the research teams led by Professor Ahn from GIST and Professor Kim from KAIST, as well as the research team from JD Bioscience Inc., was supported by the Ministry of Science and ICT, and the National New Drug Development Project. The results of this research were published by Nature Communications on January 20.
The team also presented the results of their clinical study on the candidate material coded GM-60106 targeting metabolic abnormality-related MASH* at NASH-TAG Conference 2024, which was held in Utah for three days starting on January 4, which was selected as an excellent abstract.
*MASH (Metabolic Dysfunction-Associated Steatohepatitis): new replacement term for NASH
2024.02.21 View 17918