a novel murine model of autoimmune autism mediated by complement abnormalities.

2022 Fiscal Year Final Research Report

• Project/Area Number: 20K08792
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Review Section: Basic Section 54020:Connective tissue disease and allergy-related
• Research Institution: Kitasato University (2021-2022); Hokkaido University (2020)
• Principal Investigator: Oku Kenji 北里大学, 医学部, 准教授 (70544295)
• Project Period (FY): 2020-04-01 – 2023-03-31
• Keywords: 自閉症モデルマウス / 抗C1q抗体 / C1q / 不育症

Outline of Final Research Achievements

Novel murine model of autism spectrum disorder (ASD) using complement antibody was created. Pregnant Balb/C mice were administered monoclonal anti-C1q antibody(JL-1), and the offspring mice (ASD model mice) were born. Various behavioral analyses (elevated plus maze, 3-chamber test, nose-to-nose sniffing test) were performed, and both male and female ASD model mice exhibited significantly characteristic features of ASD compared to control mice (administered control IgG or PBS). Currently, pathological observations are being analyzed.

Free Research Field

膠原病内科

Academic Significance and Societal Importance of the Research Achievements

少子化が進行する我が国では不育症と共に児の発達障害は重要な問題である。自閉症スペクトラム（ASD)は対人関係の障害や環境への適応障害を特徴とする発達障害で我が国の調整有病率は3％を超えるとの報告もある。不育症、ASDの一部に抗C1q抗体が原因な一群があると判明すると周産期の同抗体の測定や、免疫抑制療法が効果的に出産や児童の予後を改善する可能性がある。治療により少子化や児童の発達障害に介入できる可能性があることになりその社会的意義は大きいと考えられる。