Professor Kim Mikyung Wins KOFST Outstanding Paper Award... "Contributing to Research on Exercise Intensity for Brain Health"

Professor Kim Mikyung of Sahmyook University's Department of Chemistry and Life Science
Wins the 36th Outstanding Paper Award in Science and Technology
Identifies How Excessive Exercise Impairs Cognitive Function

Sahmyook University announced on November 8 that Professor Kim Mikyung of its Department of Chemistry and Life Science had received the 36th Outstanding Paper Award in Science and Technology, presented by the Korea Federation of Science and Technology Societies.

Professor Kim Mikyung of Sahmyook University, who received the Outstanding Paper Award from the Korea Federation of Science and Technology Societies for elucidating how excessive exercise contributes to cognitive decline. Sahmyook University

The award is one of the most prestigious academic honors in science and technology in Korea. Established in 1991, it recognizes and honors scientists and engineers who have published creative and outstanding research. Each academic society recommends up to two papers published in domestic journals in the previous year, and the federation selects the recipients through a review process. Professor Kim was nominated by the Genetics Society of Korea.

The award-winning paper is titled "The Key Regulatory Role of Hippocampal MCT4 in Cognitive Decline Induced by Excessive Exercise: The Involvement of Neuroinflammation." It was published online in April 2025 in Genes & Genomics, an international journal indexed in the Science Citation Index Expanded (SCIE) and published by the Genetics Society of Korea. Lee Minyoung of Sahmyook University's Department of Convergence Science and the Uimyung Neuroscience Research Institute, and Nicole von Campomayor, served as joint first authors, while Professor Kim was the corresponding author.

The study is regarded as an investigation into the molecular and biological mechanisms by which excessive exercise impairs cognitive function. Exercise is generally known to have positive effects not only on physical health but also on brain functions such as memory and learning. However, studies have also reported that excessively intense exercise may instead negatively affect cognitive function.

Schematic illustrating changes in energy metabolism in brain neurons and the mechanism underlying neuroinflammation caused by excessive exercise, as identified by a research team led by Professor Kim Mikyung of Sahmyook University. Sahmyook University

Professor Kim's team evaluated memory and learning in mice after having them exercise at different intensities. The analysis found that cognitive function declined in the group subjected to high-intensity exercise, while inflammation-related factors increased in the hippocampus, a brain region involved in memory formation and learning.

In particular, the team focused on MCT4, a lactate transporter protein involved in supplying energy to brain cells. MCT4 plays a role in transferring lactate produced by glial cells in the brain to neurons. This energy supply is important for normal memory and learning.

However, MCT4 gene expression decreased in mice that underwent excessive exercise. By contrast, mice pretreated with the anti-inflammatory drug diclofenac showed improved cognitive function and a recovery in MCT4 expression. This suggests that neuroinflammation induced by excessive exercise and changes in brain energy metabolism are closely associated with cognitive decline.

The study is expected to contribute to basic research aimed at preventing and improving cognitive decline. It may also help inform research into appropriate exercise intensity for brain health and the identification of therapeutic targets for cognitive disorders associated with neuroinflammation.

Professor Kim explained, "Previous studies have focused mainly on oxidative stress or changes in neurotrophic factors resulting from excessive exercise. This study is distinctive in that it focuses on the role of MCT4 in linking neuroinflammation with brain energy metabolism. By confirming that cognitive function and MCT4 expression recovered together following administration of an anti-inflammatory drug, we have proposed a new molecular mechanism."

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