Investigation of pathogenesis of mesial temporal epilepsy using monogenic mouse model

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460493
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Nagoya University
• Principal Investigator: Asai Masato 名古屋大学, 医学(系)研究科(研究院), 特任講師 (70543536)
• Co-Investigator(Kenkyū-buntansha): ENOMOTO ATSUSHI 名古屋大学, 大学院医学系研究科, 准教授 (20432255) ; ASAI NAOYA 名古屋大学, 大学院医学系研究科, 准教授 (80273233)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 側頭葉てんかん / 海馬硬化 / 動物モデル / ノックアウトマウス / 全般化発作 / 感覚辺縁系過剰結合

Outline of Final Research Achievements

Epilepsy is a chronic disorder characterized by recurrent seizures (by WHO's definition). The seizures are caused by sudden, usually brief, excessive electrical discharges in a group of neurons. However, the forming conditions of excessive electrical discharges are completely unknown. Mesial-temporal lobe epilepsy (MTLE), which is originated from hippocampus, is the most common form of adult epilepsy. We developed and patented monogenic MTLE mouse by ablating Girdin gene, which keeps exhibiting generalized tonic-clonic seizures and lower-level seizures for life (approximately two years) without any electrical- nor pharmacological induction. We also identified human patients in a consanguineous family with early onset epileptic seizures, caused by loss-of-function mutation in human Girdin gene (BRAIN 2016). By inferring forming conditions of excessive electrical discharges from the putative functions of Girdin protein, we proposed a new model to explain universal forms of epilepsy.

Free Research Field

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