Researchers at Catholic University of Korea discover target cells to improve cognitive dysfunction in epilepsy
At Catholic Central Medical Center, a research team led by Professor Cho Kyung-ok (corresponding author, Catholic Brain and Neuroscience Research Institute) and Dr. Inyoung Choi (first author) from the Faculty of Medicine’s Department of Pharmacology has discovered a new target cell effective in treating cognitive dysfunction associated with epilepsy.22 The day was revealed.
Epilepsy is a neurological disease whose main symptom is seizures. Temporal lobe epilepsy, which mostly affects adults, is accompanied by various psychiatric problems such as cognitive decline and emotional disturbances. To date, the development of specialized treatments for comorbid epileptic disorders has been limited because the neurobiological mechanisms have not been clearly identified.
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Professor Gyeong-ok Cho’s research group focused on “LIN28A”, a protein that is activated in the hippocampus after an epileptic seizure. The hippocampus is a part of the brain that plays an important role in memory and learning, and it has been determined that when LIN28A increases after a seizure, abnormal neurons are produced and cognitive impairment occurs.
Previous research has shown that suppressing the production of abnormal neurons can improve the cognitive dysfunction that accompanies epilepsy. As a follow-up study, a therapeutic target cell called LIN28A was discovered through this study.
As a result of deletion of the LIN28A protein using transgenic mice, it was confirmed that cognitive impairment after seizures was improved. Even when LIN28A expression was blocked without inducing seizures, no difference in cognitive impairment was found, confirming that LIN28A is a specialized molecular target for the cognitive impairment that accompanies epilepsy.
In this study, immunostaining (used to detect specific proteins using antigen-antibody reactions to proteins) targeting hippocampal dentate gyrus tissue showed that abnormally produced granule cells after seizures were significantly reduced when l LIN28A expression was blocked.
As a result of examining transcriptome analysis and RNA/protein expression to discover downstream molecular biological target cells modified by LIN28A, LIN28A-deficient epilepsy mice showed changes in the expression of serotonin receptors such as HTR4, HTR2C, and HTR1B compared to control epilepsy mice. This has been remarkably observed. Notably, HTR4 was expressed in LIN28A-expressing cells in the area where neural stem cells are primarily located.
Professor Cho said: “Among the various comorbidities of epilepsy, patients with temporal lobe epilepsy suffering from cognitive dysfunction are the most common, and the LIN28A discovered through this study will lay the foundation for the development of a treatment for the dysfunction cognitive impairment that accompanies epilepsy, which is an intractable disease in the future. “I hope we can do it,” he said.
This study was published in “JCI Insights (IF=8.0)”, a renowned international journal in the field of translational research. It was carried out with the support of the Mid-Career Researchers Support Project of the National Research Foundation of Korea, the Basic Laboratory Project, the Creative Challenges Research-based Support Project, and the Technology Development Project of the Korea Health Industry Development Institute for solving problems in the clinical fields of brain and nervous system diseases.
Journalist Jeong Yong-cheol jungyc@etnews.com
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