A Korean research team, raising the question "Which OLED light color can actually improve memory and pathological markers in Alzheimer's patients?", has identified the most effective OLED color capable of enhancing cognitive function using only light—with no drugs involved. The OLED platform developed for this study can precisely control color, brightness, flicker frequency, and exposure duration, suggesting potential future development into personalized OLED-based electroceuticals.
On the 24th, KAIST (President Kwang Hyung Lee) announced that a joint research team led by Professor Kyung Cheol Choi from the School of Electrical Engineering at KAIST and Dr. Ja Wook Koo and Dr. Hyang Sook Hoe from the Korea Brain Research Institute (KBRI) developed a uniform-illuminance, three-color OLED photostimulation technology and confirmed that "red 40-Hz light" was the most effective among blue, green, and red in improving Alzheimer's pathology and memory function.
To overcome the structural limitations of conventional LEDs—such as brightness imbalance, heat generation risk, and variability caused by animal movement—the researchers developed an OLED-based photostimulation platform that emits light uniformly. Using this platform, they compared white, red, green, and blue light under identical conditions (40-Hz frequency, brightness, and exposure time) and found that red 40-Hz light produced the most significant improvement.
In an early-stage (3-month-old) Alzheimer's animal model, improvement in pathology and memory was observed after only two days of stimulation. When early Alzheimer's model mice were exposed to one hour of light per day for two days, both white and red light improved long-term memory. Additionally, the amount of amyloid-β (Aβ) plaques—protein aggregates known as a major factor in Alzheimer's disease—was reduced in key brain regions such as the hippocampus, and levels of the plaque-clearing enzyme ADAM17 increased.
This indicates that even very short periods of light stimulation can reduce harmful proteins in the brain and improve memory function. In particular, with red light, the inflammatory cytokine IL-1β, known to exacerbate inflammation and contribute to Alzheimer's progression, decreased significantly, demonstrating an anti-inflammatory effect.
Moreover, the more plaque was reduced, the greater the improvement in memory—direct evidence that pathological improvement leads to cognitive enhancement.
In the mid-stage (6-month-old) Alzheimer's model, statistically significant pathological improvement was seen only with red light. In a two-week long-term stimulation experiment under the same conditions, both white and red light improved memory, but a statistically meaningful reduction in plaques appeared only under red light.
< The mechanism by which red OLED stimulation of neurons reduces amyloid-β in Alzheimer's model mice >
Differences at the molecular level were also clear. Under red light, levels of ADAM17 (which helps remove plaques) increased, while levels of BACE1, an enzyme responsible for producing plaques, decreased—demonstrating a dual effect of both inhibiting plaque formation and promoting plaque removal. In contrast, white light only lowered BACE1, showing more limited therapeutic effects compared to red light.
This scientifically identifies that the color of light is a key factor determining therapeutic efficacy.
To determine which neural circuits were activated by light stimulation, the team analyzed the expression of c-Fos, an immediate-early gene that is activated when neurons fire.
They found activation throughout the visual–memory circuit, extending from the visual cortex → thalamus → hippocampus, providing direct neurological evidence that light stimulation awakens the visual pathway, enhancing hippocampal function and memory.
Thanks to the uniform-illuminance OLED platform, light was evenly delivered regardless of animal movement, ensuring stable experimental results and high reproducibility across repeated tests.
This study is the first to demonstrate that cognitive function can be improved using only light, without drugs, and that Alzheimer's pathological markers can be regulated through combinations of light color, frequency, and duration.
The OLED platform developed in this study allows fine control over color, brightness, flicker ratio, and exposure time, making it suitable for personalized stimulation design in future human clinical research.
The research team plans to expand conditions such as stimulation intensity, energy, duration, and combined visual–auditory stimulation, aiming toward clinical-stage development.
< Graphical abstract for the journal ACS Biomaterials Science & Engineering – Illustration of the mechanism by which red OLED stimulation reduces amyloid-β >
Dr. Byeongju Noh (from Professor Kyung Cheol Choi's research team) said, "This study experimentally demonstrates the importance of color standardization and confirms that red OLED is the key color that activates ADAM17 and suppresses BACE1 across disease stages."
Professor Kyung Cheol Choi emphasized, "Our uniform-illuminance OLED platform overcomes the structural limitations of traditional LEDs and enables high reproducibility and safe evaluation. We expect wearable RED OLED electroceuticals for everyday use to present a new therapeutic paradigm for Alzheimer's disease."
The research findings were published online on October 25 in ACS Biomaterials Science & Engineering, a leading international journal in biomedical and materials science.
Paper Title: Color Dependence of OLED Phototherapy for Cognitive Function and Beta-Amyloid Reduction through ADAM17 and BACE1
DOI: https://pubs.acs.org/doi/full/10.1021/acsbiomaterials.5c01162
Co-authors:
Byeongju Noh, Hyun-Ju Lee, Jiyun Lee, Jiyun Lee, Ji-Eun Lee, Bitna Joo, Young-Hun Jung, Minwoo Park, Sora Kang, Seokjun Oh, Jeong-Woo Hwang, Dae-Si Kang, Yongmin Jeon, So-Min Lee, Hyang Sook Hoe, Ja Wook Koo, Kyung Cheol Choi
This research was supported by the National Research Foundation of Korea and the National IT Industry Promotion Agency under the Ministry of Science and ICT, and the Korea Brain Research Institute Basic Research Program. (2017R1A5A1014708, 2022M3E5E9018226, H0501-25-1001, 25-BR-02-02, 25-BR-02-04)
