本會學術會員 朱柏駿 及團隊研究成果獲 ITRUSST Focused Ultrasound Neuromodulation Conference (FUN)2026 國際研討會接受，以壁報（Poster）形式進行現場發表，展現臺灣在治療性超音波領域之研究實力。
本次國際研討會於 2026 年 7 月 22 日至 24 日 假 法國/巴黎 舉行，為治療性超音波領域的重要國際學術盛會，匯聚全球專家學者共同交流最新研究成果。
朱柏駿學術會員及團隊發表之研究題目為 「Low-Intensity Focused Ultrasound Modulates Hippocampal Neurogenesis and
Attenuates Neuroinflammation in a Kainic Acid-Induced Epilepsy Model」，為鼓勵會員積極參與國際學術交流、提升臺灣治療性超音波研究能見度，本會提供國際會議壁報發表補助，支持會員將研究成果帶向國際舞臺。
本會謹向朱柏駿學術會員及研究團隊表達誠摯祝賀，期盼未來持續精進研究成果，深化國際學術合作，為治療性超音波之臨床應用與科技發展貢獻更多力量。
Abstract Title:
Low-Intensity Focused Ultrasound Modulates Hippocampal Neurogenesis and Attenuates Neuroinflammation in a Kainic Acid-Induced Epilepsy Model
All Authors:
Po-Chun Chu, Jason Tan, Chen-Syuan Huang, and Hao-Li Liu
Background, Motivation and Objective
Epilepsy is characterized by aberrant neuronal activity, chronic neuroinflammation, and impaired neurogenesis within the hippocampus. Low-intensity focused ultrasound (FUS) has emerged as a promising non-invasive neuromodulation tool for treating neurological disorders.
This study aims to investigate the therapeutic potential of FUS in modulating the hippocampal microenvironment, specifically focusing on its ability to suppress seizure-related pathological markers and restore neurogenesis in a kainic acid (KA)-induced epilepsy rat model.
Methods
Nine rats were categorized into Non-KA control, KA-only, and KA+FUS groups. FUS was targeted at the hippocampus with a 0.25 Mechanical Index (MI) and a 30% duty cycle, delivered in three 10-minute sessions per day for a total of six sessions over two weeks (Fig. 1A). To evaluate the therapeutic effects, histological analysis was performed to quantify NeuN expression for seizure-related neuronal activity, IBA-1 for microglial-mediated neuroinflammation, and Doublecortin (DCX) for the rate of hippocampal neurogenesis within the targeted region.
Results/Discussion
Histological analysis indicated that FUS application altered the pathological state of the hippocampus. NeuN-positive signaling, which reflects seizure-related neuronal activity, reached 1.12 ± 0.12 in the KA-only group and was 1.02 ± 0.12 in the KA+FUS group (Fig. 1B).
Regarding neuroinflammation, the expression of IBA-1, a marker for microglial activation, measured 1.27 ± 0.29 in the KA-only group and 1.20 ± 0.09 in the KA+FUS group (Fig. 1C).
Assessment of the neurogenic niche showed that KA administration reduced DCX levels to 0.37 ± 0.03, while FUS treatment resulted in an increase to 0.89 ± 0.18 (Fig. 1D). These data show that repeated FUS stimulation modifies epileptic circuits by reducing inflammatory responses and supporting the survival of immature neurons. The recovery of DCX-positive cells indicates that FUS promotes a regenerative environment within the targeted hippocampal region. Consequently, FUS serves as a method for restoring neural homeostasis, suggesting its potential in the long-term management of epilepsy-related brain pathology.